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SYRINGOMYELIA 


AN  ESSAY  TO  WHICH  WAS  AWARDED  THE  ALK4RENGA  PRIZE 
OF   THE  COLLEGE  OF  PHYSICIANS  OF  PHILA- 
DELPHIA FOR    THE   YEAR   1895 


BY 


GUY   HINSDALE,  A.M.,  M.D. 


fellow   of   the  college  of   physicians  of  philadelphia    and   of   the   american   academy   of 
medicine;  member  of  the  American  neurological  association  and  of  the  Philadelphia 
neurological  society  ;  member  of  the  american  climatoi.ogical  association  j 
honorary  member  of  the  pueblo  county  medical  society  of  colorado  j 
assistant  physician  to  the  orthopedic  hospital  and  infirmary 
for  nervous  diseases  ;   attending  physician  to  the  pres- 
byterian   orphanage   and    to    the    out-patient 
department  op  the  pkesbytekian  hospital 
in  philadelphia,   etc. 


PHILADELPHIA 

THE  INTERNATIONAL  MEDICAL  MAGAZINE  COMPANY 

1897 


f 


Copyright,   1897, 

BY 

The  International  Medical  Magazine  Co.\ 


TO 

DR.  S.  WEIR   MITCHELL, 

AS  A  SLIGHT  TRIBUTE  OF  RESPECT  AND  AS  A   RECOGNITION  OF 

MANY  SERVICES  RENDERED 

TO  THOSE   WHO  HAVE  BEEN  ASSOCIATED  WITH  HIM 

IN   PUBLIC   AND   PRIVATE   PRACTICE. 


PREFACE. 

The  author  would  call  attention  to  the  extraordinary  amount  of  litera- 
ture which  has  appeared  during  the  last  few  years  with  reference  to  syringo- 
myelia. We  place  in  evidence  a  bibliography  the  most  complete  that  has 
thus  far  been  collected,  amounting  to  five  hundred  and  fourteen  references. 
Of  these,  two  hundred  and  thirty  have  been  reported  from  Germany  and 
Austria,  France  has  furnished  one  hundred  and  sixty-six,  while  eighty-five 
have  appeared  in  English.  We  have  gone  to  the  original  sources  and  have 
analyzed  one  hundred  and  eighteen  cases  which  have  been  published  since 
1890.  The  essay  is  based  on  a  study  of  these  and  of  the  two  unpublished 
cases  which  we  have  added  to  the  list,  and  particularly  the  publications  of 
Bruhl  and  Guinon,  of  Paris,  Hoffmann,  of  Heidelberg,  and  Schlesinger,  of 
Vienna.  The  essay  was  originally  printed  in  the  November  and  Decem- 
ber, 189G,  and  January,  1897,  numbers  of  the  INTERNATIONAL  Medical 
Magazine. 

[The  synopsis  of  published  cases  which  accompanied  the  essay  as 
presented  is  not  included  in  this  publication.] 


Digitized  by  the  Internet  Archive 

in  2010  with  funding  from 

Open  Knowledge  Commons 


http://www.archive.org/details/syringomyeliaOOhins 


TABLE   OF   CONTENTS. 


Preface v 

History  and  definition 3 

Ili-tology  and  pathology 8 

Symptomatology 17 

Etiology 45 

Forms  of  syringomyelia 47 

Association  with  other  diseases 50 

Diagnosis 54 

Course  of  the  disease  and  prognosis .  57 

Treatment 57 

Two  unpublished  cases 57 

Bibliography CO 

[ndex 73 


SYRINGOMYELIA. 


THE  ALVARENGA  PRIZE  ESSAY  OF  THE  COLLEGE 

OF  PHYSICIANS  OF  PHILADELPHIA 

FOR  THE  YEAR  1895. 


It  is  over  one  hundred  and  fifty  years  since  Morgagni  and  Santorini 
observed  and  recorded  the  existence  of  an  abnormal  cavity  in  the  spinal 
cord. 

Portal  in  the  year  1800,  and  Rachetti  in  1816,  also  noted  this  strange 
phenomenon,  which  had  from  time  to  time  excited  the  curiosity  of  anatomists 
of  the  seventeenth  and  eighteenth  centuries.  The  pathological  condition 
passed  without  a  distinctive  name  until,  in  1837,  Ollivier,  of  Angers,  called 
the  affection  "syringomyelia,"  by  which  it  has  since  been  generally  desig- 
nated. The  word  itself  is  from  the  Greek  ffupiyyuat,  "  to  become  hollow,"' 
and  [ioeXds,  "  marrow,"  a  combination  which  clearly  expresses  the  macro- 
scopic appearance  when  section  is  made  of  a  typical  specimen.  The  next 
step  was  the  discovery  in  1859,  by  Stilling,  that  the  spinal  cord  is  normally 
provided  with  a  central  canal  which  is  constant  throughout  life.  Yirchow 
and  Leyden  then  looked  upon  all  cavities  in  the  cord  as  expansions  of  the 
normal  central  canal,  and  termed  the  condition  "  hydroniyelia."  Ollivier  is 
said  to  have  attributed  to  the  affection  very  little  pathological  significance, 
and  certainly  did  not  connect  the  condition  with  any  clinical  symptoms; 
thus  all  writers  down  to  within  twenty  years  or  even  less  gave  very  little 
value  to  the  condition  other  than  as  being  merely  a  pathological  curiosity 
and  of  little  importance.  It  transpired,  however,  that  in  cases  where  these 
cavities  were  found  at  an  autopsy  the  clinical   histories  bore  a  strong  resem- 

3 


4  GUY    HINSDALE,    M.D. 

blance  in  some  respects.  Disorders  of  sensation  had  been  observed  ;  burns 
and  wounds  received  during  later  years  had  been  sustained  without  pain; 
certain  muscles  had  wasted  and  there  had  been  the  symptoms  of  muscular 
weakness  to  such  an  extent  as  to  interfere  with  the  customary  avocations. 
It  thus  became  evident  that  the  cavity  and  the  surrounding  histologic 
change  were  accountable  for  a  train  of  clinical  symptoms  which  had  not 
been  heretofore  attributed  to  a  definite  locality  in  the  central  nervous  system. 
The  first  differentiation  of  these  cases  was  made  when  a  pathological 
condition,  evidently  congenital,  was  distinguished  from  a  cavity  acquired  in 
later  life  as  the  result  of  accidental  causes  or  the  growth  of  new  formations 
in  the  spinal  cord.  For  the  congenital  affection  it  has  been  found  conven- 
ient to  retain  the  name  hydromyelia;  but  for  the  cavities  secondarily  pro- 
duced, even  though  they  may  be  considered  as  remotely  due  to  a  develop- 
mental defect  dating  as  far  back  as  intra-uterine  existence,  it  has  generally 
been  the  custom  to  use  the  term  syringomyelia,  as  originally  proposed. 

Fig.  1. 


Hydromyelia  from  a  child  two  years  old,  with  encephalocele  and  absence  of  cerebellum.  (From 
Gowers,  after  Leyden.)  In  A,  cervical  region,  the  central  canal  is  large,  lined  with  epithelium,  and 
from  it  a  median  Assure  extends  backward  nearly  to  the  periphery  of  the  cord,  limited  by  a  layer  of 
homogeneous  tissue,  more  abundant  at  the  posterior  limit.  In  B,  lower  down,  the  fissure  is  enlarged  to 
a  cavity  of  considerable  size,  while  in  C  it  is  still  larger,  and  the  posterior  columns  are  reduced  to  a 
narrow  zone  between  the  layer  of  tissue  which  bounds  the  cavity  and  the  gray  substance. 


The  definition  which  we  adopt,  and  to  which  every  author  will  doubtless 
assent,  is  that  syringomyelia  is  a  chronic  affection  of  the  spinal  cord  charac- 
terized anatomically  by  the  pathological  formation  of  cavities  in  its  sub- 
stance, and  clinically  by  peculiar  disturbances  of  sensibility  associated  with 
trophic  disorders.  The  seat  of  the  primary  lesion  may  extend  as  high  as 
the  medulla  or  as  far  downward  as  the  lumbar  region ;  the  seat  of  the 
secondary  changes  is  peripheral,  involving  the  muscles,  the  bones,  the 
cellular  tissue,  the  skin,  etc. 

Two  other  terms  have  been  proposed,  but  they  have  not  been  accepted 
by  the  profession.  One  is  "  myelite  cavitaire,"  of  Joffroy  and  Achard, 
which  indicates  the  secondary  nature  of  the  cavity,  but  it  is  objectionable  on 
account  of  the  term  myelitis,  which,  in  the  usual  acceptation  of  the  term, 
misrepresents  the  primary  pathological  condition. 

The  other  name,  proposed  by  Sachs  and  Armstrong,  is  myelosyringosis. 
The  term  is  no  doubt  a  correct  one  for  the  condition,  but  it  is  not  so 
euphonious  as  syringomyelia,  and  will  probably  never  come  into  use. 

It  was  a  distinct  step  in  advance  when  it  was  recognized  by  Hallopeau, 
in  1869,  that  it  was  not  so  much  the  cavity  per  se  that  was  the  main  element 


SYRINGOMYELIA. 


in  the  pathological  condition,  but  rather  that  the  cellular  changes  which 
take  place  in  the  cord  constitute  the  primary  lesion,  and  that  the  dilatation 
of  the  cavity  is  only  secondary.  Hallopeau's  explanation  was  that  a 
myelitis  occurred  with  sclerosis  of  the  periependymal  tissue;  as  the  latter 
gave  way  the  central  canal  was  thus  secondarily  excavated  into  a  large  cavity. 

This  statement  seemed  beyond  criticism  until  further  studies  revealed 
cavities  in  the  cord  independent  of  the  central  canal  and  not  even  communi- 
cating with  it. 

Simon,  of  Paris,  contributed  much  to  the  elucidation  of  the  subject, 
which  had  now  become  greatly  confused  owing  to  the  successive  change  of 
views.  His  studies,  which  were  published  in  1875,  called  attention  to  the 
coexistence  of  the  cavity  with  vascular  tumors,  to  which  he  gave  the  name 
of  "gliomes  telangiectasiques,"  and  rightly  claimed  that  the  cavity  resulted 
from  softening  of  the  glioma  and  absorption  of  the  degenerated  structure. 

In  Simon's  opinion,  which  is  now  generally  adopted,  hvdromyelia  was 
reserved  for  "  la  dilatation  et  Vhydropisie  du  canal  d'ependyme,  affection  en 
tout  comparable  a  I'hydrociphalie"  and  to  use  the  word  syringomyelia  to 
designate  "  les  cavites  et  productions  hystiques  que  Von  pent  rencontrer  dans  la 
moelle  independamment  du  canal  central" 

Much  more  attention  has  been  directed  in  later  years  to  the  study  of 
the  symptomatology  of  syringomyelia.  The  train  of  clinical  symptoms 
and  their  explanation  by  post-mortem  studies  furnish  one  of  the  most 
beautiful  subjects  for  the  student  of  clinical  medicine  and  pathology.  The 
statement  that  a  diagnosis  can  only  be  made  at  the  autopsy  has  been  rele- 
gated to  historv.  The  rigorous  efforts  of  Morvan  to  establish  an  identity 
for  the  disease,  which  he  described  as  "panaris  analgesique"  or  " paresie 
analgesique  a  panaris  des  extremites  super ieures"  have  likewise  been  un- 
successful, for  the  best  observers  are  now  nearly  united  in  classifying  this 
affection  as  one  of  the  forms  or  types  of  syringomyelia  and  not  a  disease 
sui  generis. 

V\<;.  2. 


Transverse  section  "f  achici  -Ik. win-  medullary  canal  (T.  C.)  beginning  u> 
(Prom  Kolliker.) 

The  various  forms  of  this  interesting  disease,  which  is  already  the  sub- 
ject of  a  vast  amount  of  literature,1  will  be  considered  more  particularly  in 
succeeding  chapters. 

Histology  and  Pathology. — In  the  development  of  the  spinal  cord  of 
the  embryo  the  germinal  space  or  area  in  its  very  earliest  stage  takes  on  an 


1  In  the  bibliography  prepared  by  the  author  there  are  500  references. 


6  GUY    HINSDALE,    M.D. 

elongated  form,  a  central  longitudinal  line  called  the  primitive  groove. 
The  sides  of  this  primitive  furrow  are  composed  of  two  longitudinal  ridges 
of  the  external  layer  or  fold  (epiblast)  of  the  blastoderm. 

These  close  in  so  as  to  form  a  canal  constituting  the  fundamental  cen- 
tral canal  of  the  cord,  the  fourth  ventricle  (which  is  only  partially  en- 
closed), arid  the  ventricles  of  the  brain.  The  walls  of  this  canal  are  thinner 
in  front  and  behind  than  at  the  sides,  and  the  epithelium  of  the  central 
canal  is  derived  from  the  same  external  layer  (epiblast)  of  the  blastoderm, 
the  nerve  elements  themselves  being  derived  from  the  middle  layer,  the 
mesoblast,  subjacent  to  this  epithelium.  The  central  canal  is  at  first  closed 
behind  by  only  a  thin  layer  of  cells  which  meet  across  the  middle  line,  the 
remnant  of  this  fissure  forming  the  posterior  median  fissure,  the  closure 
occurring  from  behind  forward  as  the  median  parts  of  the  posterior  columns 
develop. 

The  nature  of  the  cellular  constituents  of  the  cord  must  be  also  under- 
stood in  an  explanation  of  the  pathological  changes.  All  the  parts  consist 
first  of  embryonal  cells,  or  plasmatic  cells  as  they  are  sometimes  called, — 
embryonic  cells,  because  they  are  the  same  in  the  adult  as  they  were  in  the 
embryonic  stage.  Such  cells  easily  undergo  transformation,  however, 
decaying,  perhaps,  or  furnishing  new  forms  that  become  pathological. 

As  the  embryo  develops,  some  of  the  embryonal  cells  are  transformed 
into  the  nerve-elements,  the  cells  of  the  gray  matter  taking  shape  before 
the  fibres  of  the  white  columns.  Others  persist,  forming  the  neuroglia  and 
the  gelatinous  gray  substance  continuous  with  it  around  the  cord,  at  the 
posterior  root  fissure  and  around  the  central  canal  (Gowers). 


Fig.  3. 


Representing  the  posterior  end  of  the  spinal 
canal  open.  The  anterior  and  lateral  columns 
have  been  formed.  The  posterior  columns  en- 
croach on  the  canal. 


Fig.  4. 


Development  of  the  cord  com- 
plete by  the  growth  of  the  posterior 
median  column.  The  spinal  canal 
is  closed. 


It  is  therefore  to  be  noted  that  the  cells  surrounding  the  central  canal 
and  extending  to  the  posterior  root  fissure  are  the  very  cells  most  prone  to 
undergo  transformation.  The  central  canal  is  finally  located  in  the  anterior 
part  or  middle  of  the  gray  commissure.  It  is  barely  discernible  to  the 
naked  eye  either  as  a  slit  extending  laterally  or  antero-posteriorly,  or  circu- 
lar in  section,  or  may,  in  exceptional  cases,  be  normally  closed  by  the 
epithelium  which  usually  lines  its  wall. 

The  development  of  the  cord  may  stop  at  several  stages  short  of  comple- 


SYRINGOMYELIA.  7 

tion.  The  central  canal  may  remain  abnormally  large  in  proportion  as  the 
junction  of  the  dorsal  portion  of  the  cord  occurs  at  any  position  between  the 
normal  one  and  the  hindmost  limit  of  the  posterior  fissure. 

The  boundaries  of  the  canal  may  be  symmetrical  or,  if  the  junction  has 
taken  place  unevenly,  a  portion  of  the  original  posterior  fissure,  or  an  offset 
from  it,  may  be  thrown  sideways  into  either  the  right  or  left  posterior 
column,  decentring  the  cavity  and  giving  it  an  asymmetrical  outline. 

Fig.  5. 


Syringomyelia.   Case  ol  E.  Asmus.   <  larity  extends  from  the  third  cervical  to  the  tenth  dorsal  segment. 
TIm'  right  posterior  horn  chiefly  affected.    The  anterior  horns  intact.    Specific  history. 

It  has  been  suggested  also  that  in  some  cases  the  cord  may  be  normally 
developed  as  far  as  external  appearance  goes,  but  may  contain  an  undue 
amount  of  embryonic  neuroglia,  in  which  a  hemorrhage  or  liquefactive  de- 
generation may  easily  be  determined  by  degrees  of  violence  which  would  be 
insufficient  to  affect  a  normal  cord. 

It  can  therefore  readily  be  understood  that  in  some  cases  of  syringo- 
myelia we  may  deal  with  a  congenital  weakness   if  not  an  actual  defect,  a 


8  GUY    HINSDALE,    M.D. 

developmental  irregularity  in  the  distribution  of  cellular  elements;  that, 
furthermore,  the  filling  up  of  congenital  or  acquired  spaces  in  the  neuroglial* 
element  with  the  products  of  some  new  formation,  glioma  for  example,  and 
the  exercise  of  pressure  from  within  outward,  will  react  upon  the  gray 
matter,  so  that  as  it  degenerates  the  intrinsic  symptoms  of  the  disease  pre- 
sent themselves,  and  as  later  the  white  matter  itself  undergoes  transforma- 
tion, the  extrinsic  symptoms  are  added  to  the  list. 

Pathology. — On  examining  the  cord  as  it  lies  in  the  vertebral  canal  the 
general  appearance  may  be  entirely  normal.  The  meninges  are  apparently 
healthy,  but  upon  opening  the  dura  mater,  if  the  case  be  well  marked,  the 
cord  will  bear  a  strong  resemblance  to  a  large  blood-vessel  filled  with  a 
moderate  quantity  of  fluid,  having  walls  reduced  in  thickness  in  proportion 
as  the  gray  matter  has  been  destroyed.  On  pressure  it  is  found  to  lack 
resistance,  being  soft  and  fluctuating.  In  extreme  cases  it  may  be  of 
ribbon-like  appearance.  The  cervical  enlargement  is  relatively  great,  or  at 
whatever  locality  a  glioma  may  be  present  there  may  be  a  fusiform  swelling. 
The  cervical  and  upper  dorsal  regions  are  the  usual  seats  of  the  affection. 

The  external  appearance  is  not  always  so  characteristic  in  cases  of 
moderate  degree. 

On  cross-section  the  distinctive  features  of  the  disease  are  apparent  to 
the  naked  eye.  In  successive  sections  of  a  well-marked  specimen  we  may 
trace  the  glioma  and  its  cavity  throughout  its  vertical  extent. 

Fig.  6.1 


%-.■■  . 

Syringomyelia.— Upper  cervical  region.  Here  the  cavity  extends  far  across  the  cord,  almost  sym- 
metrically on  either  side.  The  gliomatous  formation  extends  out  along  the  posterior  horns,  almost 
cutting  off  the  posterior  columns  from  the  rest  of  the  cord.  The  lateral  tracts  are  much  degenerated, 
especially  the  right,  and  the  right  direct  pyramidal  tract.  Remnants  of  the  anterior  horns  can  be  made 
out  as  narrow  projections  in  front  of  the  cavity  (the  left  alone  is  shown  in  the  drawing  - ;  they  contain 
only  a  few  multipolar  cells  degenerated.  The  anterior  parts,  especially,  of  the  posterior  columns,  are 
degenerated.  But  little  trace  of  posterior  root-zone.  The  gliomatous  tissue  extends  almost  entirely 
around  the  cavity  as  a  rim  or  circle. 

The  cavity  is  usually  single,  but  there  may  be  several  cavities  inde- 
pendent of  each  other  or  intercommunicating.  The  cross-section  of  the 
cavity  is  generally  elliptical,  or  merely  a  narrow  slit  with  the  long  diameter 

1  The  author  wishes  to  express  his  indebtedness  to  Dr.  James  Hendrie  Lloyd 
for  the  use  of  these  valuable  illustrations,  which  were  executed  from  photographs 
by  Dr.  William  M.  Gray,  of  the  Army  Medical  Museum,  Washington. 


SYRINGOMYELIA. 


Fig.  7. 


^'•Vi;,»>r';-,v')'  :-'-"-v.M».'  ■>.,  ;,-'; )■■■■  :Jvvv;  '•,'''■'■■' 


This  drawing  represents  very  well  a  section  from  the  mid-dorsal  region.  (The  image  is  reversed  ) 
The  cavity  is  to  the  right  (left  in  figure),  and  follows  out  the  posterior  horn  quite  to  the  periphery.  The 
right  lateral  tract  is  very  much  degenerated,  and  the  left  is  rather  more  so  than  is  shown  in  the  draw- 
ing. The  right  anterior  horn  is  also  practically  destroyed.  The  left  anterior  horn  preserves  its  shape, 
and  under  the  microscope  some  motor  cells  are  visible  in  it.  The  posterior  columns  show  degenerated 
fibres  scattered  through  them. 


Fig.  8. 


Syringomyelia.— Cervical  enlargement,    The  cavity  here  begins  to  trend  towards  the  right  side 
(left  in  the  photograph),    [t  is  lined  with  a  glioma  as  of  the  central  canal  can  be 

seen  in  a  group  of  epithelial  cells  in  front  of  the  cavity  und  in  our  side  of  Its  normal  position.    Ii  pre- 

larly  the  outlines  of  a  double  canal     [tdoi  ir  In  the  photograph.    The  ai 

white  commi  erved.    The  gray  matter  is  strel  ty.andonly 

a  few  multipolar  cells  are  visible  (very  Indistinct  In  this  photograph)  In  the  anterior  horns.  The  lateral 
pyramidal  tract  is  deeply  degenerated,  and  the  direct  pyramidal  tract  slightly  bo.  The  posti  rior  horns 
and  root-zones  cannot  be  well  distinguished. 


10 


GUY    HINSDALE,    M.D. 


transverse  (Figs.  6,  8,  9,  10).  The  shape  of  the  cavity  varies  very  largely, 
and  its  long  axis  may  lie  in  almost  any  direction,  very  commonly  extending 
obliquely  in  the  direction  of  one  of  the  posterior  horns.     (Fig.  7.) 

The  dimensions  of  cavities  vary  greatly  in  different  cases  and  at  differ- 
ent levels  in  the  same  case,  measuring  one  millimetre  or  less  up  to  almost 
the  entire  thickness  of  the  cord,  and  usually  attaining  their  maximum  in 
the  cervical  region.     While  the  cervical  and  upper  dorsal  portions  of  the 

Fig.  9. 


Syringomyelia.— Cervical  enlargement.  Cervical  region  next  below  Fig.  8.  Cavity  trends  still 
farther  to  right.  (In  this  the  image  is  not  reversed.)  The  anterior  horn  can  be  well  distinguished.  It 
contains  more  multipolar  cells  than  the  former  section,  but  under  a  high  power  they  are  seen  to  be  de- 
generated. Otherwise  the  appearances  are  much  the  same  as  in  section  from  which  Fig.  8  is  taken. 
The  direct  pyramidal  tract  on  the  right  is  more  degenerated  than  on  the  left.  The  anterior  portion, 
especially,  of  the  columns  of  Goll  are  involved  in  gliomatosis. 


cord  are  the  usual  seat  of  cavities,  they  have  been  observed  in  the  lumbar 
enlargement  alone. 

Position. — The  cavity  itself  always  lies  in  the  gray  matter  primarily. 
It  occupies  very  frequently  the  position  of  the  central  canal  in  the  peri- 
ependymal tissue.  It  is  often  observed  posterior  to  the  canal  in  the  gray 
substance  forming  the  posterior  commissure,  and  may  extend  throughout 
one  or  both  of  the  anterior  or  posterior  horns,  reaching  thus  to  the  very 
margin  of  the  cord.  In  such  cases  the  cavity  is  asymmetrical,  lying  chiefly 
in  either  the  right  or  the  left  half.     The  white  matter  in  moderate  cases  is 


SYEIXGOM  YELI A . 


11 


unaffected,  but  where  the  cavity  is  large,  and  pressure  from  the  glioma  has 
become  great,  the  white  matter  is  in  its  turn  involved,  being  crowded  to 
the  periphery  and  more  or  less  unable  to  carry  on  its  functions.  The  an- 
terior columns  of  the  white  substance  preserve  their  integrity  to  the  last. 
We  are  unable  to  point  to  a  single  case  in  which  these  have  been  affected. 
Since  the  defect  is  originally  posterior,  it  is  natural  that  the  columns  of 


Fig.  10. 


Syringomyelia.— Upper  dorsal  region.  The  cavity  trends  to  the  right  (image  not  reversed).  The 
glioinatous  tissue  extends  down  both  posterior  hums.  All  around  It  the  white,  as  well  as  gray,  matter 
nerated,  especially  in  the  direct  and  crossed  pyramidal  tracts  (mure  marked  in  the  right).  The 
anterior  parts  of  the  posterior  columns  also  are  affected.  The  gray  matter  is  almost  entirely  destroyed, 
except  the  anterior  horns,  which  are  seen  as  mere  small  projections  in  front  of  the  cavity.  They  con- 
tain l.ut  few  cells. 

Goll  and  Burdach  should  be  the  first  of  the  white  matter  to  undergo  a 
change.  The  trophic  columns  of  Clark,  at  the  neck  of  the  posterior  roots 
(gray  matter),  are  also  often  affected.  The  initial  situation  of  the  glioma 
is  about  the  central  canal,  extending  thence  to  Clark's  column,  and  then  to 
the  anterior  and  posterior  horns. 

In  fifty-six  cases  where  autopsies  were  made  the   lesion  was  located  as 
follows  : 

( '  \-i .-  |  Baumler  . 

Posterior  horns 21      Left  posterior 6 

Anterior  home 11      Right  anterior 5 

Right  posterior 5      Lefl  anterior 5 


12 


GUY    HINSDALE,    M.D. 


The  lateral  columns,  and  particularly  the  pyramidal  tracts  when  involved, 
as  they  occasionally  are,  produce  paraplegia.  The  invasion  of  the  columns 
of  Burdach  and  Goll  gives  rise  to  sensory  phenomena,  while  the  degenera- 
tion of  Clark's  column  probably  is  accountable  for  the  trophic  changes. 


Fig.  11. 


Syringomyelia—  Lumbar  enlargement.  The  cord  here  presents  a  striking  contrast  to  its  appear- 
ance higher  up.  Its  general  shape  and  size,  as  well  as  those  of  its  gray  matter,  are  normal.  The  an- 
terior horns  are  large  and  well  supplied  with  motor  cells.  The  posterior  horns  and  root-zones  are 
plainly  seen.  In  but  two  features  does  it  present  very  marked  abnormal  appearances;  and  these,  in 
view  of  the  diseased  state  of  the  cord  higher  up,  are  full  of  interest.  First,  the  lateral,  or  crossed, 
pyramidal  tracts,  which  are  here  small  and  have  come  to  the  periphery,  are  degenerated.  Second,  the 
region  of  the  central  canal,  in  the  posterior  gray  commissure,  shows  distinctly  gliomatous  change.  Al- 
ready the  central  canal  is  obliterated,  but  no  gliomatous  cavity  has  yet  taken  the  place  of  the  normal 
one.  Dr.  Lloyd  remarks  that  this  proves  very  beautifully  that  the  cavity  in  syringomyelia  is  not  a  mere 
expansion  of  the  normal  canal.  On  the  contrary,  the  normal  canal  does  not  exist  any  longer,  and  its 
place  is  taken  by  the  remains  of  its  columnar  epithelial  cells,  which  have  undergone  coagulation  ne- 
crosis with  loss  of  their  characteristic  columnar  appearance.  This  group  of  broken-down  cells  is  sur- 
rounded by  the  gliomatous  mass,  which  at  this  level  occupies  but  a  small  space  in  the  gray  commissure. 
We  see  here,  probably,  an  early  stage  of  the  gliomatous  process  at  the  lowest  point  of  its  downward 
progression  in  the  cord.    Slight  degeneration  is  seen  here  in  the  posterior  columns  near  the  periphery. 

If  the  new  formation  give  rise  to  pressure  in  an  extreme  degree  there 
may  be  hemorrhages,  inflammation,  and  evidences  of  degeneration.  In 
such  an  event  it  would  be  the  gray  matter  of  the  cord  that  would  show  the 
hemorrhage  and  inflammation,  while  the  white  columns  would  undergo 
degeneration.  This  latter  would  be,  as  a  rule,  ascending,  for  it  is  the  pos- 
terior and  lateral  columns  that  are  most  frequently  attacked.  Inasmuch  as 
sensory  disorders  constitute  the  corner-stone  of  the  diagnosis  of  syringo- 


SYRINGOMYELIA.  13 

rnyelia,  it  is  quite  likely  that  the  proportion  of  cases  in  which  the  posterior 
columns  are  affected  (sixty-two  per  cent,  according  to  Wichraann)  is  consid- 
erably greater  than  has  been  recognized  hitherto.  In  the  one  hundred  and 
eighteen  cases  published  which  we  have  carefully  examined,  nine  cases,  or 
eight  per  cent.,  showed  degeneration  of  the  posterior  columns,  while  a  larger 
majority  showed  sensory  changes.  It  should  be  remembered,  however, 
that  it  is  possible  for  syringomyelia  to  exist  without  any  sensory  disorder. 
In  a  case  of  Schlesinger's  (VI.  Monograph,  1895),  there  was  no  anaesthesia 
of  any  form,  but  an  autopsy  revealed  a  cavity  extending  nearly  the  entire 
length  of  the  cord.  Ascending  degeneration  was  found  in  Lloyd's  case,  in 
which  the  patient's  motor  symptoms  were  more  marked  on  the  right  side, 
and  the  left  pyramid  degenerated  above  the  cavity. 


W'- 


Mb 


^rc 


\ 


r? '  :" 


Ascending  Degeneration  in  Syringomyelia.  (Medulla  Oblongata,  Lloyd.)— Ng,  nucleus  funiculi 
gracilis;  tfc,  nucleus  funiculi  cuniati;  /'.funiculus  cuniatus;  Sub  g,  substantia  gelatinosa;  2Ti,  acces- 
sory nerve ;  DC,  direct  cerebellar  tract :  l',  ascending  root  of  fifth  nerve;  I'll,  posterior  born  ;  a.  (Sowers' 
tract ;  Ah.  anterior  horn  ;  D,  decussal  Ion  of  pyramids ;  Pyr,  left  pyramid. 

The  light,  unshaded  areas  are  degenerated.  The  central  canal  is  surrounded  wiib  gliomatous  ma- 
terial.    The  fibres  of  the  accessory  nerve  are  too  diagrammatic.     They  are  not  so  distinct  in  the  section. 

The  section  shown  in  Fig.  12  was  made  at  about  the  region  of  the  de- 
cussation of  the  pyramids.  The  central  canal,  lined  with  epithelium,  is 
seen.  It  is  surrounded  by  gliomatous  material,  which  has  not  yet  begun  to 
break  down  into  a  cavity,  although  under  the  microscope  it  is  seen  to  be 
brittle  and  friable.  The  decussating  fibres  are  seen  and  the  remnants  of 
the  anterior  horns  cut  off  by  them,  lying  to  their  outer  side.  It  is  to  be 
noted  that  the  fibres  running  towards  the  right  are  much  more  numerous 
then  those  running  in  the  opposite  direction  ;  also,  that  the  left  pyramid  is 
degenerated. 

In  another  case,  which    recently  died  in   the  Philadelphia  Hospital 
Fig.  15), ascending  degeneration  of  the  pyramidal  tracts  was  found  by  Der- 


14  GUY    HINSDALE,    M.D. 

cum  and  Spiller.     In  this  case  sections  were  made  from  the  level  of  nearly 
every  spinal  root  and  from  many  spinal  ganglia. 

By  the  microscopic  examination  degeneration  of  the  crossed  pyramidal 
tract  was  found  as  high  as  the  substantia  reticularis  of  the  second  cervical 
segment  and  of  the  direct  pyramidal  as  high  as  the  motor  decussation  upon 
the  right  side,  and  for  a  short  distance  of  the  crossed  pyramidal  upon  the 
left.     This  was  believed  to  be  ascending  on  account  of  the  following  facts  : 

1.  Absence  of  any  microscopic  lesion  above  the  medulla  oblongata. 

2.  Degeneration  of  the  crossed  and  direct  pyramidal  tracts  on  the  same 
side  of  the  cervical  cord,  intense  in  the  lower  cervical  region  near  the  lesion, 
and  diminishing  gradually  in  intensity  in  the  cervical  segments,  and  finally 
becoming  very  indistinct  in  the  upper  cervical  region. 

3.  Absence  of  all  degeneration  in  the  anterior  pyramids. 

4.  Long  duration  of  a  chronic  process. 

While  certain  associative  fibres  may  be  considered  degenerated  in  these 
columns,  the  entire  anterolateral  column  contains  such  fibres,  and  the  de- 
generation was  notably  in  the  area  occupied  by  the  crossed  and  the  direct 
pyramidal  tract.  This  ascending  sclerosis  was  probably  in  greater  part  due 
•  to  destruction  of  motor  fibers  deprived  of  their  function. 

Degeneration  of  the  direct  cerebellar  tracts  and  of  the  tracts  of  Gowers 
was  traced  as  far  as  the  inferior  peduncles  of  the  cerebellum.  Intense 
pachymeningitis  was  noticed  from  the  second  lumbar  segment  to  the  exit  of 
the  third  dorsal  roots.  The  arthropathy  of  the  right  shoulder  was  not  due 
to  any  special  changes  in  the  cord  or  spinal  ganglia.  The  posterior  roots 
were  not  affected  even  where  the  pachymeningitis  was  most  intense ;  the 
anterior  roots  at  one  part  of  the  dorsal  cord  were  degenerated.  In  the  entire 
cervical  region  as  high  as  the  second  cervical  segment  the  cavity  was  limited 
to  the  right  posterior  horn.  The  gliosis  extended  from  the  extreme  end  of 
the  conus  terminalis  to  the  second  cervical  segment.  The  microscopic 
examination  explained  satisfactorily  the  symptoms  observed  in  life. 

In  this  case  the  disease  dated  from  a  strain  of  the  back;  three  years 
later  there  were  severe  pains  in  the  legs,  a  band-like  pain  about  the  lower 
part  of  the  chest,  weakness  in  the  lower  limbs,  and  a  spastic  gait.  Com- 
plete paraplegia  with  contractures,  more  marked  on  the  right  side,  wasting 
of  the  lower  limbs,  paralysis  of  bladder  and  rectum  developed  later.  Cuta- 
neous sensibility  was  lost  in  the  legs  and  upon  the  trunk  as  high  as  the 
nipple  on  the  right  side  and  a  little  above  the  umbilicus  on  the  left.  The 
sense  of  temperature  was  absolutely  lost  over  the  right  arm,  the  right  shoul- 
der, and  the  right  side  of  the  neck,  and  also  upon  the  adjacent  part  of  the 
right  sideof  the  trunk  above  the  nipple-line.  There  was  some  analgesia  of 
the  right  arm. 

It  is  only  in  exceptional  cases  that  pressure  is  exerted  laterally,  and,  on 
account  of  interference  with  the  functions  of  the  crossed  pyramidal  tracts, 
that  spastic  phenomena  develop. 

Marked  atrophy  is  an  indication  of  excavation  of  the  anterior  horns,  and 


SYRINGOMYELIA.  15 

its  seat,  whether  in  the  upper  or  lower  extremities,  is  an  index  of  the  ver- 
tical extent  of  the  lesion.  In  advanced  cases  the  lesion  passes  beyond  the 
cervical  cord  and  involves  the  medulla.  This  is  made  evident  by  difficul- 
ties of  speech  and  deglutition,  and  even  mental  degeneration  and  other 
symptoms  of  bulbar  disease  arising  from  disturbances  of  innervation  of  the 
glossopharyngeal,  hypoglossal,  pneumogastric,  and  spinal  accessory  nerves. 
When  the  nerves  themselves  are  affected,  we  may  have  the  evidences  of 
neuritis.1 

The  contents  of  the  cavity  vary  considerably  in  color  and  consistence. 
In  some  cases  the  liquid  is  clear,  analogous  to  the  cerebro-spinal  fluid ;  in 
other  cases  it  may  be  described  as  a  hyaline  jelly  perfectly  clear  or  of  a 
turbid  or  yellowish-brown  hue.  It  may  be  bloody,  thick,  and  viscid,  or 
contain  gelatinous  flakes.  It  never  ruptures  outward,  as  it  is  not  subject  to 
any  very  great  internal  pressure. 

The  walls  of  the  cavity  are  smooth  and  glossy  as  a  rule,  but  in  ex- 
ceptional cases  are  rough,  shreddy  and  uneven,  and  of  a  slightly  yellowish 
color. 

The  new  formation,  which  is  the  starting  point  of  syringomyelia,  is 
gliomatous.  This  may  be  defined  as  a  neoplastic  hyperplasia  of  the  gray 
matter, — a  glioma.  It  has  been  called  by  Cornil  and  Ranvier  a  neuroglial' 
sarcoma.  According  to  Joffroy  and  Achard,  Hallopeau  and  Erckholt, 
after  an  inflammatory  hyperplasia  or  myelitis  a  cavity  forms  from  the  re- 
traction of  the  sclerosed  periependymal  tissue  from  the  distinctive  tendency 
of  the  hyperplasia,  or  may  arise  from  softening  consequent  on  thrombosis 
of  the  inflamed  vessels.  Considerable  stress  is  laid  on  the  vascular  origin 
of  the  cavity,  some  authors,  such  as  Langhans,  Stadelmann,  and  Steudener, 
asserting  that  the  cavity  results  from  periependymal  oedema,  or  from 
hemorrhage  with  secondary  absorption,  or  from  colloid  degeneration  of  the 
vessels. 

Joffroy  and  Achard's  term,  myUite  cavitaire,  is  entirely  reconcilable  with 
the  views  held  by  Simon,  Westphal,  Roth,  Blocq,  and  Schultze,  that  the 
syringomyelia  is  due  to  a  degeneration  of  the  elements  of  a  neoplasm, — a 
glioma.  The  differences  of  opinion  are  rather  discrepancies  of  terminology. 
It  may  be  said  briefly  that  the  usual  course  of  arteritis  in  syphilis  and  in 
disseminated  sclerosis  is  towards  a  diffuse  sclerosis  and  not  to  cavities.  We 
do  not  meet  with  cavities  in  the  system  scleroses.  The  argument,  however, 
that  syringomyelia  does  not  result  from  a  myelitis  or  a  central  softening  of 
the  cord  by  endarteritis  because  we  do  not  meet  with  syringomyelic  cavities 
in  the  scleroses  of  the  cord  has  been  shown  by  Dr.  Byroru  Bramwell  to  be 
unfounded. 

The  glioma  has  its  seat  in  the  gray  substance,  particularly  the  peri- 
ependymal region,  and  affects  chiefly  the  gelatinous  substance  of  Rolando, 

1  See  Alexis  Thomson's  case  for  neuritis  of  the  suprascapular  and  circumflex 
nerves,  Edinburgh  Hospital  Reports,  1894. 


16  GUY    HINSDALE,    M.D. 

which  acts  as  an  intercellular  cement  on  the  gray  matter.  It  is  of  a 
yellowish-brown  color  and  of  a  rather  firm  consistence.  The  latest  teaching 
of  the  French  school  is  that  this  mass  is  the  result  principally  of  an  agglom- 
eration of  large  cells,  which  are  more  or  less  crowded  together,  sending  out 
ramifications  which  by  their  interlacing  enclose  small  spaces.  The  cells 
themselves  form  small  masses  of  protoplasm,  which  are  grouped  centrally 
or  peripherally,  and  stain  conspicuously  the  ordinary  reagents.  The 
trabecule  are  long  and  delicate,  slightly  thickened  at  certain  points.  In 
the  net- work  of  filaments  the  granular  elements  are  enclosed  as  well  as  free 
cells  and  fine  fibres,  together  with  numerous  pigment  granules,  which  give 
the  growth  a  distinctive  color.  The  reticular  tissue  is  well  supplied  with 
capillaries. 

The  cavity  is  in  most  cases  lined  by  a  thin  membrane,  which  to  the 
naked  eye  is  glossy  and  of  a  yellowish  hue.  It  consists  of  a  delicate  mem- 
brane of  neurogliar  tissue  composed  of  branching  neuroglia  cells  of  various 
sizes  and  with  small  spheroidal  and  oval  cells  embraced  in  a  net-work  of 
fibres.  These  elements  may  be  either  densely  packed  together  or  loosely 
arranged.  In  other  cases  the  cavity  has  no  limiting  membrane  or  we  may 
have  such  a  membrane  present  in  one  portion  of  the  cavity  but  absent  at 
other  portions.  The  process  of  liquefaction  readily  takes  place  in  the 
limiting  membrane.  Small  holes  are  sometimes  observed  in  the  wall, — 
spheroidal  cavities  which  have  been  evidently  produced  by  liquefactive  de- 
generation with  disappearance  of  the  neuroglia  cells.  Van  Gieson  shows 
that  these  changes  in  the  glia-cells  are  not  caused  by  the  action  of  the 
hardening  agents,  since  the  degenerating  cells  are  not  scattered  uniformly 
throughout  the  cord,  but  are  noticeable  wherever  there  is  much  hyperplasia 
of  neurogliar  tissue. 

In  a  typical  case  the  tumor  is  composed  of  closely-packed  masses  of 
spindle-shaped  and  oval  cells  associated  with  filaments  arranged  in  strands 
between  and  around  numerous  blood-vessels  which  are  surrounded  by  a 
close-textured,  sparingly  nucleated  sheath  of  neuroglia  filaments.  The 
cells,  when  isolated,  comprise  glia-cells,  together  with  granular,  rounded,  or 
spindle-shaped  non-branching  cells,  resembling  the  cells  of  sarcomata.  The 
liquefying  product  will  be  found  to  consist  of  fluid,  fibrin,  hsematogenous 
pigment,  and,  in  places,  of  disintegrated  tumor  cells.  Liquefactive  de- 
generation of  the  glia-cells,  gliomatous  tumors,  constitutes  one  of  the  charac- 
teristic features  of  syringomyelia.  In  a  given  case  we  may  find  obliteration 
of  the  central  canal ;  at  the  same  time  no  gliomatous  cavity  has  taken  the 
place  of  the  normal  one.  While  the  canal  does  not  exist,  we  find  in  its 
place  the  remains  of  its  columnar  epithelial  cells  broken  down  in  a  coagula- 
tion necrosis  with  a  loss  of  their  characteristic  columnar  appearance.  At 
other  levels  the  fully-formed  cavity  will  be  observed. 

It  should  be  borne  in  mind  that  not  every  change  visible  under  the 
microscope  was  actually  present  in  life.  Irregularities  of  outline,  for  exam- 
ple, are  very  often  due  to  the  manipulation  of  the  cord  in  the  process  of 


SYRINGOMYELIA.  17 

removal  aud  subsequent  examination.  Too  much  stress  should,  therefore, 
not  be  placed  on  such  distortions.  The  case  of  Gyurman  has  been  cited  by 
Van  Gieson  as  one  of  these  examples  of  artefacts  mistaken  in  some  respects 
for  pathological  change.  Dr.  Byrom  Bramwell *  has  shown  by  microscopic 
sections  from  two  ordinary  cases  of  myelitis  that  cavity-formation  with  a 
surrounding  dense  membrane  does  occur,  but  that  specimens  of  central 
gliosis  from  another  case,  which  he  very  carefully  prepared,  show  that  the 
cavity  was  formed  by  breaking  down  in  the  process  of  preparation. 

Symptomatology. — The  symptomatology  of  syringomelia  has  been  placed 
upon  an  established  basis  during  only  the  last  fifteen  years.  Previous  to 
that  period  the  clinical  symptoms  had  not  been  grouped  and  classified  and 
given  their  proper  value  so  as  to  be  of  any  service  to  the  clinician  in  recog- 
nizing the  disease.  Its  identity,  judging  it  by  a  series  of  post-mortem 
records,  has  been  established  by  a  system  of  a  posteriori  reasoning,  so  that 
we  are  in  possession  of  a  definite  train  of  symptoms  that  have  enabled  the 
clinician  to  declare,  in  turn,  the  pathological  changes  which  are  present  in  a 
given  case,  particularly  if  the  clinical  symptoms  are  well  marked. 

These  symptoms  arrange  themselves  as  follows : 

I.  Intrinsic  symptoms. 

1.  Symptoms  of  anterior  poliomyelitis,  and  motor  symptoms  (atrophy). 

2.  Symptoms  of  median  poliomyelitis  (the  central  gray  substance  of 

the  cord). 

(1)  Trophic  disorders. 

(2)  Deviations  of  the  spinal  column. 

(3)  Vasomotor  disturbances. 

(4)  Disorder  of  the  sphincters. 

(5)  Ocular  symptoms. 

(6)  Bulbar  symptoms. 

3.  Symptoms  of  posterior  poliomyelitis. 

II.  Extrinsic  symptoms. 

1.  Sclerosis  of  the  lateral  columns.     Spastic  phenomena. 

2.  Sclerosis  of  the  posterior  columns.     Tabetic  phenomena. 

By  means  of  this  convenient  classification,  which  we  owe  to  the  late 
Professor  Charcot,  we  may  study  the  symptoms  in  order. 

I.  The  intrinsic  symptoms  are  related  to  the  gray  substance  itself. 

1.  Degeneration  of  the  cells  of  the  anterior  horns  manifests  itself  by 
muscular  atrophy.  This  feature  of  syringomyelia  is  rarely  absent,  and  is 
almost  as  characteristic  as  disturbance  of  sensation.  Atrophy  was  one  of 
the  first  of  the  clinical  symptoms  that  appeared  prominently  in  a  review  of 
those  cases  in  which  an  autopsy  revealed  syringomyelia.  Indeed,  many  of 
these  cases  had  been  diagnosticated  as  progressive  muscular  atrophy.8 


1  Medico-Chirurgical  Transactions,  Ivlinbur^h,  18!W-(»4. 

2  Examples  are  found  in  the  cases  of  Gull,  Clarke,  Beevor,  Westphal,  Ivahler  and 
Pick,  Schultzc,  Dreschfeld,  and  Schuppel. 


18 


GUY    HINSDALE,    M.D. 


The  most  frequent  form  of  atrophy  is  of  the  type  Aran-Duchenne.  The 
small  muscles  of  the  hand,  the  interossei,  the  thenar  and  hypothenar  emi- 
nences, appear  to  be  the  regions  most  frequently  involved.  The  atrophy 
invades  the  forearm  and  the  arm,  the  muscles  of  the  shoulder-girdle  and 
trunk,  occasionally  involving  a  portion  of  the  tongue,  almost  always  sparing 

the  face. 

Fig.  13. 


A  case  of  syringomyelia,  showing  atrophy.    (From  the  Philadelphia  Hospital.) 

Whether  general  or  unilateral,  the  atrophy  in  these  cases  is  always  of 
spinal  origin,  and  by  a  knowledge  of  spinal  localization  we  are  enabled  by 
the  initial  motor  symptoms  and  by  their  progress  to  determine  very  closely 
the  seat  of  lesion.  Valuable  charts  have  been  prepared  and  published  by 
Dr.  M.  Allen  Starr  and  Dr.  C.  K.  Mills  as  guides  in  spinal  localization. 


SYRINGOMYELIA.  19 

They  have  been  made  from  data  drawn  from  studies  in  comparative 
anatomy,  physiological  experiment,  and  records  of  spinal-cord  diseases, 
especially  from  the  study  of  anterior  poliomyelitis,  transverse  myelitis,  and 
syringomyelia. 

The  muscles  of  the  lower  extremity  are  not  involved  by  any  means  as 
frequently  as  those  of  the  upper  limb.  Paraplegia  is,  however,  not  a  rare 
symptom.1 

The  gait  is  frequently  much  disturbed.  It  is  slow  and  in  extreme  cases 
so  uncertain  that  it  has  been  mistaken  for  that  of  intoxication.  Particularly 
is  this  the  case  when  the  white  matter  of  the  cord  is  affected,  where  tabetic 
or  spastic  symptoms  have  supervened.  If,  in  addition,  the  medulla  has 
been  involved  with  consequent  thickness  of  speech  it  is  evident  that  unfor- 
tunate mistakes  of  this  kind  would  occur.  Such  have  been  recorded  by 
Hoffmann,  Raich  line,  F.  Taylor,  and  Haumann. 

Electrical  Reactions. — The  atrophied  muscles  are  prone  to  undergo  quan- 
titative and  qualitative  changes  in  their  electrical  reactions.  The  opinion  is 
now  becoming  more  common2  that  the  sign  of  reaction  of  degeneration  has 
lost  much  of  the  diagnostic  value  which  we  have  for  a  long  time  accorded  it, 
inasmuch  as  it  is  met  with  in  affections  that  are  purely  muscular,  as,  for 
example,  pseudo-hypertrophic  muscular  paralysis,  and  as,  on  the  other  hand, 
we  note  its  absence  in  nervous  amyotrophies  of  advanced  type.  In  syringo- 
myelia there  is  great  diversity  in  this  respect  in  different  cases.  In  the  one 
hundred  and  eighteen  cases  which  we  have  analyzed  the  reaction  of  degen- 
eration in  the  atrophied  muscles  was  recorded  in  twenty-one  cases.  While 
no  doubt  many  cases  were  not  examined  in  this  regard,  we  may  safely  say 
that  R.  D.  is  not  found  by  any  means  so  frequently  in  syringomyelia  as  in 
atrophy  consequent  on  neuritis.  It  is  quite  common,  however,  to  find 
quantitative  changes  in  syringomyelia,  there  being  diminution  and  some- 
times total  disappearance  of  electrical  excitability.  In  one  of  Midler's  cases 
the  muscles  presented  a  normal  appearance  apparently  in  no  way  atrophic, 
and  yet  there  was  very  great  diminution  of  faradic  and  galvanic  excitability. 

Schlesinger  and  Frank!  Ilochwart  have  called  attention  to  a  case  which 
was  under  treatment  by  direct  applications  of  the  faradic  current  to  the 
biceps,  exhibiting  a  peculiar  undulation  in  that  muscle  when  stimulated, 
and  which  continued  to  show  this  phenomenon  during  the  entire  course  of 
treatment. 

Fibrillary  Tremors. — The  affected  muscles  also  present  another  phenom- 
enon,— viz.,  fibrillary  twitching  or  tremor.  True  tremors,  as  observed  in 
paralysis  agitans  and  in  hysteria,  are  not  observed  in  syringomyelia,  but  we 
find  frequent  mention  of  a  frequent  and  intense  fibrillary  twitching.  In 
our  analysis  of  one  hundred  and  eighteen  cases  this  feature  is  mentioned 
thirty  times. 

1  Cases  of  Westphal,  Schultze,  Grasset,  Chabanne,  and  Baichline  form  exceptions. 
*  See  Guinon's  remarks  in  the  Traits  de  M6decin,  vol.  iii.,  1894. 

2 


20  GUY    HINSDALE,    M.D. 

2.  Symptoms  of  median  poliomyelitis. 
This  important  group  of  symptoms  embraces  those  which  we  seem  jus- 
tified in  attributing  to  an  alteration  of  the  central  gray  substance  of  the 
cord.  The  later  continental  writers,  including  Bruhl,  have  adopted  the 
classification  which  we  give  below.  While  in  some  respects  questions  may 
arise  as  to  the  localization  of  some  of  the  symptoms  in  this  group,  with  our 
present  knowledge  we  are  not  able  to  definitely  relegate  them  elsewhere. 

(1)  Trophic  disturbances. 

(2)  Deviations  of  the  spinal  column. 

(3)  Vasomotor  disorders. 

(4)  Affections  of  the  sphincters. 

(5)  Oculo-pupillary  changes. 

(6)  Bulbar  symptoms. 

(1)  The  trophic  disorders  of  syringomyelia  affect  four  tissues,  viz., — 
(a)  The  skin  and  mucous  membranes. 
(6)  The  subcutaneous  cellular  tissue. 

(c)  The  joints. 

(d)  The  bones. 

(a)  Trophic  alterations  of  the  skin  are  commonly  observed  in  syringo- 
myelia, and  may  be  of  all  grades,  from  a  slight  glossy  condition  to  extensive 
necrosis  or  gangrene.  These  changes  are  usually  confined  to  the  extremi- 
ties affecting  the  atrophied  structures,  and  are  prone  to  occur  in  the  anaes- 
thetic regions:  occasionally  there  is  a  tendency  to  hypertrophy  of  the  skin 
with  formation  of  dense  fibrous  tissue  (Case  CXII.).1  It  is  common  to 
observe  scaling,  cracking,  and  the  formation  of  deep  fissures  that  are  the 
seat  of  ulcers  that  become  chronic  and  refuse  to  heal.  These  cracks  are 
commonly  seated  in  the  palm  of  the  hand,  and,  although  the  fissures  them- 
selves are  frequently  painless,  the  chronic  ulcerations  are  so  unsightly  that 
they  are  often  the  occasion  of  the  patient's  presenting  himself  for  treatment. 
These  cracks  furnish  a  ready  pathway  for  infection,  and  particularly  in 
syringomyelia  of  Morvan's  type  they  lead  to  actual  deformity.  The  accom- 
panying plate  from  a  case  of  H.  Curschmann's  illustrates  very  well  this 
condition.  The  nails  become  striated,  crack,  and  suppurate  at  the  matrix. 
As  seen'in  the  plate,  some  have  fallen  off,  and  the  remaining  stumps  with 
their  horny  appendages  present  a  repulsive  appearance.  The  resemblance 
between  the  observed  trophic  disorders  of  the  skin  and  scleroderma  are  not 
uncommonly  noted  by  observers.  Syringomyelia  has  been  mistaken  for 
pemphigus,  on  account  of  the  spontaneous  bullae  or  phlyctenules  that  are 
liable  to  occur  on  the  hands  and  feet.  These  phenomena  are  liable  to  be 
persistent,  and  to  give  rise  to  obstinate  ulcerations  that  are  difficult  to  heal, 
and  show  a  tendency  to  spread.  In  a  case  of  Neuberger's  there  were  as 
many  as  thirty  separate  areas  of  ulceration,  of  irregular  outline  and  varying 


1  Yerhoogen  and  Vandervelden's  case,  in  which  a  cavity  was  found  independent 
of  the  spinal  canal. 


SYRINGOMYELIA. 


21 


size  all  over  the  body.  Besides  this,  there  were  pigmented  areas  in  places, 
and  radiating  cicatrices  in  other  situations.  In  this  case  there  was  a  syphi- 
litic history,  but  the  autopsy  showed  a  syringomyelia.  The  mucous  mem- 
brane of  the  mouth  had  been  so  extensively  involved  that  speech  was 
disturbed,  the  small  vesicles  which  appeared  along  the  right  border  and  tip 


Fig.  14. 


Trophic  changes  in  syringomyelia. 


of  the  tongue  ruptured  and  left  small  ulcerated  areas  that  were  extremely 
painful,  and  rendered  impossible  the  ingestion  of  solid  food.  These 
patches  were  at  first  of  circular  outline,  and  covered  with  a  yellowish  de- 
posit and  surrounded  by  a  reddened  areola,  but  after  a  time  they  tended  to 
become  confluent.  At  a  later  period  the  left  border  of  the  tongue  also  be- 
came affected.  In  a  little  while  the  entire  organ  became  enormously 
swollen.  In  the  intervals  between  the  paroxysms  ulceration  sometimes  took 
place  in  the  fissures  present.  At  the  time  of  the  attacks  there  were  also 
pricking  sensations  in  the  face.  Sometimes  the  tonsils  were  swollen  and 
the  seat  of  a  yellowish  deposit.  The  condition  affecting  the  mucous  mem- 
brane of  the  mouth  and  pharynx  was  believed  to  be  pemphigus,  non- 
syphilitic  in  character.  On  one  occasion  an  eruption  of  vesicles  was 
observed  upon  the  extensor  aspect  of  the  right  hand,  and  on  another  occa- 
sion a  similar  eruption  on  the  middle  toe  of  the  left  foot.  Upon  post-mortem 
examination  the  tongue  was  found  swollen,  fissured,  and  ulcerated.  The 
epiglottis  was  enlarged  and  reddened.  The  entrance  to  the  larynx  was 
closed  by  intense  oedema  of  the  ventricular  bands.     The  mucous  membrane 


22  GUY    HINSDALE,    M.D. 

of  the  larynx  was  thick  and  rugous,  in  places  eroded,  and  here  and  there, 
particularly  upon  the  arytenoid  cartilages,  presenting  frothy,  yellowish 
secretions,  probably  derived  from  the  rupture  of  pre-existing  vesicles. 
The  mucous  membrane  of  the  trachea  was  hyperaemic,  swollen,  and  covered 
with  frothy  secretion. 

(b)  The  subcutaneous  cellular  tissue  undergoes  well-marked  trophic 
changes.  One  type  of  syringomyelia  (that  of  Morvan)  is  distinguished  by 
painless  panaritia,  whitlows,  or  felons.  These  appearances  are  usually 
associated  with  the  palmar  cutaneous  fissures  previously  referred  to. 

There  are  phlegmons  and  abscesses,  more  or  less  extensive,  seated  in  the 
arms,  the  axilla?,  and  the  palms  of  the  hands.  Perforating  ulcer  may  also 
develop.  In  a  case  of  Le  Fort's,  in  which  panaris  had  existed,  and  small 
swellings  like  boils  had  appeared  on  the  forearm,  shoulder,  and  abdominal 
walls,  gangrenous  areas  appeared  in  the  external  and  upper  portion  of  the 
left  forearm  and  on  the  posterior  and  outer  part  of  the  shoulder. 

All  these  trophic  lesions  of  subcutaneous  tissues  are  often  serious,  if  not 
by  their  extent,  at  least  by  their  refusal  to  heal.  They  almost  always  leave 
behind  permanent  cicatrices  and  more  or  less  deformity  or  mutilation. 

Wherever  trophic  disturbances  like  panaris  occur  there  is  occasionally  a 
subjective  sense  of  cold ;  in  other  cases  the  skin  assumes  a  cyanotic  hue  or, 
on  the  other  hand,  a  diffused  redness  of  the  skin  with  sense  of  burning. 
In  these  cases  the  surface  temperature  is  sensibly  elevated,  and  a  surface 
thermometer  may  record  from  7°  to  9°  C.  more  than  when  normal  areas 
are  tested. 

Neuropathic  oedema  may  occur  in  a  generalized  manner  or  localized  in 
a  single  part,  as,  for  example,  in  the  dorsum  of  the  hand.  In  one  of  Ver- 
hoogen  and  Vandervelden's  cases  (No.  6)  there  was  a  cyanotic  oedema  of 
the  ankles  when  the  patient  assumed  the  erect  position. 

Roth  has  described  cases  with  "tumeurs  pateuses"  which  are  examples 
of  neuropathic  oedema  seated  in  the  connective  tissue.  They  presented 
pitting  on  pressure  and  were  not  associated  with  any  discoloration  of  the 
skin. 

(c)  Arthropathy. — Just  as  in  tabes  so  in  syringomyelia,  it  is  not  unusual 
to  find  affections  of  the  joints.  Indeed,  they  occur  rather  more  frequently 
than  in  locomotor  ataxia.  In  our  analysis  of  one  hundred  and  eighteen 
cases  we  find  arthropathies  in  thirty-eight  or  thirty-two  per  cent,  of  cases. 
They  may  occur  spontaneously  without  trauma,  appearing  suddenly  without 
accompanying  fever  or  pain.  The  shoulder-  and  elbow-joints  are  favorite 
sites  in  this  respect,  affording  a  contrast  to  tabetic  arthropathy  in  which  in 
about  seventy-five  per  cent,  of  cases  we  find  the  lower  extremities  involved. 
The  syringomyelic  arthropathies  are  usually  seated  in  the  upper  extremities. 
It  is  liable  to  occur  at  an  early  stage,  and  taken  in  connection  with  sensory 
disturbances  constitutes  an  important  and  early  sign  of  the  disease. 

In  Schlesinger's  ninety-seven  cases  of  syringomyelia  with  arthropathy 
we  have  the  following  distribution  : 


SYRINGOMYELIA. 


23 


Schlesinger's  Cases. 

Shoulder-joint 29 

Elbow-joint 24 

Wrist-joint 18 

Thumb 2 

Hip 4 

Knee 7 

Ankle 7 

Jaw 4 

Steruo-clavicular 2 

Total 97 

The  arthropathy  may  consist  of  a  simple  hydrarthrosis.  The  joint 
swells  and  leads  the  patient  to  consult  a  surgeon,  sometimes,  rather  thau  a 
physician.  It  is  not  generally  painful,  and  may  become  quite  aggravated 
without  the  patient  being  aware  of  it.  There  may  be  a  subsidence  for  a 
time  and  then  an  increase  of  deformity.  After  swelling  of  the  joint  and 
subsequent  disappearance  of  the  fluid  the  articulation  is  loosened  by  re- 

Fig.  15. 


Arthropathy  of  the  shoulder  in  syringomyelia,    I  Alexis  Thomson  I 


taxation  of  the  ligaments,  and  it  is  quite  easy  to  produce  luxation.  The 
epiphyses  become  friable;  spontaneous  luxation  may  occur  with  the  growth 
of  enormous  osteophytes.  Motion  at  this  stage  is  accompanied  by  crack- 
ling sounds,  but  the  movements  arc  not,  as  a  rule,  painful  to  the  patient. 

Tn  a  characteristic  case  which  had  been  under  observation  for  years  in 
the  Philadelphia  Hospital,  and  studied  by  Dr.  Dercum  and  others,  the 
right   shoulder-joint    began  to  swell,  and    from   rupture  of  the  capsular  lig- 


24  GUY    HINSDALE,    M.D. 

ament  cellulitis  with  redness  and  local  heat  was  produced,  but  with  little  or 
no  pain.  In  extension  the  humerus  assumed  the  position  of  a  subglenoid 
luxation.     Death  was  due  to  exhaustion. 

At  the  autopsy,  in  1896,  the  capsule  of  the  right  shoulder-joint  was 
found  much  thickened  and  roughened  on  the  inner  surface.  The  head  of 
the  humerus  had  disappeared,  the  bone  having  been  eroded  to  some  little 
distance  below  the  surgical  neck.  A  cystic  tumor  was  found  in  the  axilla 
containing  a  friable  fatty  material.  The  surface  of  the  glenoid  cavity  was 
much  eroded,  roughened,  and  porous;  it  was  abnormally  large,  and  exten- 
sive bony  deposits  had  taken  place  along  its  edges.  The  coracoid  process 
exhibited  a  thick  and  firm  accretion  around  its  entire  edge.1 

Shoulder-joints  have  even  been  excised  2  without  the  use  of  an  anaes- 
thetic, and  in  one  instance  the  patient  himself  occasionally  used  to  evacuate 
fluid  from  his  elbow  with  a  pair  of  scissors.  A  typical  case  of  this  kind 
has  been  recently  published  in  full  by  Mons.  J.  B.  Charcot.  The  patient, 
a  female,  aged  fifty-seven,  had  furnished  a  characteristic  picture  of  syrin- 
gomyelia, in  which  the  left  upper  extremity  was  the  seat  of  the  dissociation 
symptom.  The  right  arm  and  forearm  retained  feebly  their  sensation. 
Scoliosis  and  lordosis  were  marked.  In  the  course  of  time  this  patient 
left  the  hospital,  and  three  years  after  the  publication  of  Critzman's  account 
of  the  case  it  came  again  under  observation.  It  transpired  that  in  1892 
she  had  a  fall,  first  striking  the  left  atrophied  shoulder  and  then  the  right 
shoulder,  which  was  the  better  and  which  was  only  slightly  disturbed  as  to 
sensation.  She  continued  to  use  her  arm,  but  not  so  well  as  before,  but  at 
the  end  of  three  weeks  it  had  swollen  considerably  and  movement  was 
more  difficult.  The  right  shoulder-joint  was  the  seat  of  an  effusion  and 
half  a  litre  of  fluid  was  drawn  by  aspiration.  A  luxation  received  at  the 
time  of  the  fall  was  then  easily  reduced,  but  recurred,  and  crackling  sounds 
of  the  joint  were  noted.  The  head  of  the  humerus  became  atrophied  and 
deformed,  so  much  so  that  dislocation  could  be  produced  at  will  in  all 
directions.  Pain  had  never  been  very  noticeable  in  this  joint ;  it  was 
present  at  times,  especially  under  manipulation,  but  was  transient  and 
easily  borne.  It  was  particularly  the  crackling  which  disturbed  and  irri- 
tated the  patient. 

The  vast  majority  of  subjects  of  syringomyelia,  whether  male  or  female, 
belong  to  the  laboring  classes,  and  in  such  patients  repeated  injury  of  a 
joint  is  liable  to  occur,  especially  if  the  sense  of  pain  has  been  impaired  or 
abolished.  In  many  of  these  cases  it  requires  only  a  slight  accident  to 
give  rise  to  affections  of  the  joints.  It  is  not  uncommonly  observed  that 
in  cases  of  trophic  disturbances  of  the  skin  a  slight  mechanical  or  thermic 
irritation  is  often  followed   by  active  vasomotor  troubles  and  by  various 


*For  description  of  pathological  changes  in  the  spinal  cord,  see  page  13. 
2Sokoloff's  case  and  Czerny's  case. 


SYRINGOMYELIA.  25 

symptoms  such  as  would  not  occur  from  similar  exciting  agents  in  healthy 
persons.1 

It  must  not  be  concluded,  however,  from  such  premises  that  syringomy- 
elic arthropathies  are  of  traumatic  origin.  Volkmann  maintained  that 
such  was  the  case  in  tabes,  but  his  view  has  not  been  accepted,  and  the  pre- 
vailing opinion,  based  on  clear  evidence,  is  that  they  are  distinctly  trophic 
lesions.  The  obscure  nature  of  the  arthropathy  is  borne  out  by  the  various 
theories  that  have  been  formulated  for  its  explanation.  That  they  are 
syphilitic  as  Striimpell  has  claimed  we  cannot  admit,  nor  can  we  concede 
that  they  are  rheumatic  in  origin.  Buzzard's  theory  that  they  are  due  to 
an  invasion  of  the  medulla  oblongata  because,  as  he  claimed,  they  were  co- 
incident with  gastric  and  laryngeal  crises  is  equally  untenable.  This  author 
fortified  his  position  by  arbitrarily  assigning  to  the  medulla  a  trophic  cen- 
tre for  the  bones  and  joints. 

Believing  with  Charcot,  Blocq,  Hoffmann,  Xissen,  and  Marinesco  that 
the  arthropathy  of  syringomyelia  is  entirely  analogous  in  its  origin  to  that 
of  tabes,  we  deem  it  entirely  fair  to  use  the  same  arguments  in  support  of 
the  explanation  of  the  nature  of  syringomyelic  arthropathy  that  have  been 
adduced  to  explain  that  of  tabes. 

Among  the  earliest  investigations  of  this  subject  was  that  of  Charcot 
and  Joffroy  in  1870  (q.v.).  They  examined  the  spinal  cord  of  a  woman 
who  had  had  locomotor  ataxia  for  ten  years,  with  a  large  tabetic  arthropa- 
thy of  the  left  shoulder,  and  with  complete  destruction  of  the  head  of  the 
humerus.  In  addition  to  a  characteristic  sclerosis  of  the  posterior  columns, 
there  was  a  remarkable  atrophy  of  the  left  anterior  horn  in  the  cervical 
region,  with  destruction  of  many  cells  particularly  in  the  posterior  external 
group.     At  other  levels  the  anterior  horns  were  normal. - 

In  another  instance  Charcot  and  Joffroy  found  an  atrophy  of  the  ante- 
rior horn  of  the  lumbar  cord  coincident  with  arthropathy  of  the  knee  of  the 
same  side,  and  they  believed  them  to  be  in  the  relation  of  cause  and  effect. 
Later  investigations  by  Pierret  (1870),  de  Lionville  (1874),  and  Seeligmi'd- 
ler  seem  to  support  this  view ;  but  those  of  Bourceret  (1875),  Raymond 
(1875),  Pities  and  Vaillard  {Revue  de  3Iedeeine,  1886),  and  Pavlides  (1888) 
have  afforded  negative  observations.  Talamon  also  failed  to  find  any  lesion 
of  the  anterior  horns  in  several  autopsies  in  cases  of  spinal  arthropathy. 
Pitres  and  Vaillard  did  find,  however,  in  four  cases  of  tabetic  arthropathy 
alterations  of  the  periarticular  nerves,  and  even  of  the  capsular  filaments, 
and  from  these  observations  tiny  announced  the  theory  of  the  peripheral 
nervous  origin  of  the  affection,  in  which  they  have  been  supported  by 
Siemerling. 

Marinesco  has  examined  the  spinal  cord  (Revue  Neurologique,  July  30, 


casi  -  of  •' urgena  ami  Marinesco. 
'-'  It  will  lie  noticed  in  this  connection  that  the  arthropathies  of  syringomyelia 

are  chiefly  in  the  upper  extremities,  ami  that  the  usual  Bite  ofthe  central  lesion  18  in 

the  lower  cervical  ami  upper  dorsal  regions. 


26 


GUY    HINSDALE,    M.D. 


1894),  the  crural  nerves,  and  articular  filaments  in  a  case  of  double  tabetic 
arthropathy.  The  cord  showed  a  system-sclerosis  of  the  posterior  columns, 
having  its  greatest  intensity  in  the  lumbar  region.  In  this  situation  there 
remained  in  the  posterior  columns  only  a  few  scattered  fibres  in  the  cornu- 


Fir;.    16 


Arthropathy  in  general  paresis.    (From  a  ease  of  Dr.  Lloyd,  in  the  Philadelphia  Hospital.) 


commissural  zone.  There  were  still  a  few  fibres  scattered  ihrough  the 
other  zones  of  the  posterior  columns.  The  zone  of  Lissauer  was  com- 
pletely degenerated,  as  well  as  the  posterior  horns.  The  anterior  horns 
were  normal  throughout  the  entire  lumbar  region.  The  crural  nerves  on 
both  sides  showed  well-marked  degeneration,  which  appeared  particularly 


SYRINGOMYELIA.  27 

in  certain  bundles  of  fibres, — in  other  words,  there  were  atrophied  medul- 
lated  nerve-fibres.     The  articular  nerves  had  also  degenerated. 

Finally,  in  a  well-marked  case  of  arthropathy  in  general  paresis,  studied 
by  J.  H.  Lloyd,  an  illustration  of  which  is  presented  for  comparison,  it 
could  not  be  affirmed  that  a  direct  connection  was  apparent  between  the 
cord  lesions  and  the  arthropathies,  but  the  opinion  was  expressed  that  this 
connection  existed  probably  by  way  of  the  nerve-roots.  The  spinal  cord 
in  this  case  showed,  first,  partial  posterior  sclerosis,  and,  second,  sclerosis  of 
the  motor  tracts  from  one  hemisphere, — i.e.,  the  crossed  pyramidal  tract  on 
the  right  side  and  part  of  the  direct  pyramidal  tract  on  the  left  side.  The 
multipolar  cells  of  the  anterior  horns  in  the  region  examined  (mid-dorsal 
region)  did  not  present  very  marked  changes. 

We  are  very  much  in  need  of  a  further  study  of  the  nature  of  syringo- 
myelic arthropathy. 

The  arthropathies  of  syringomyelia,  as  well  as  of  tabes,  have  been  ar- 
ranged under  two  heads:  first,  the  atrophic  form,  which  is  the  rarer;  and, 
second,  the  hypertrophic  form,  more  usually  seen,  and  which  resembles  in 
some  respects  the  lesions  of  arthritis  deformans. 

Recent  investigations  lead  to  the  opinion  that  a  lesion  of  the  articular 
sensory  nerves  is  accountable  for  these  arthropathies.  Goldscheider's  ob- 
servations show  that  the  articular  surfaces  are  sensitive  to  mechanical  and 
thermic  irritations.  Recent  studies  by  Golgi  show  that  numerous  sensory 
nerve-corpuscles  exist  in  the  tendons  themselves,  but  no  one  has  yet  de- 
scribed trophic  nerves  passing  from  the  centre  to  the  periphery  in  a  manner 
analogous  to  the  nerve-fibres  of  muscles  and  glands.  "We  may  then  un- 
derstand how,  in  the  atrophic  form  of  arthropathy,  at  least  the  articular 
surfaces  of  the  bones,  deprived  of  their  sensory  nerves  by  degenerative  pro- 
cesses, are  thereby  unable  to  recognize  the  adverse  conditions  to  which  they 
may  be  subjected.  The  nutritive  function  being  dependent  on  intact  sen- 
sory innervation  is,  therefore,  abated  as  the  communication  with  the  vaso- 
motor centres  is  gradually  lost.  The  resulting  impoverishment  of  the 
blood-supply  results  in  the  wasting  and  reabsorption  of  the  constituents  of 
the  articulation."  ' 

On  the  other  hand,  an  ingenious  theory  is  advanced  to  explain  the  hy- 
pertrophic form.  "  It  is  a  recognized  fact  that  in  healthy  individuals  there 
are  certain  spontaneous  compensations  of  nutrition.  Applying,  now,  the 
same  principles  in  pathologic  conditions,  it  may  be  urged  that  in  some  forms 
of  arthropathy,  for  example,  portions  of  an  articulation  are  deprived  of  a 
regular  nutritive  circulation  because  their  centripetal  nerve-supply  ia  im- 
paired. Thus  it  may  occur  that  the  neighboring  portions  remaining  unaf- 
fected enjoy  a  compensatory  increase  of  nutrition  corresponding  to  what  has 
been  denied  the  affected  regions."  However  this  may  be,  hypertrophies  do 
occur  in  the  neighborhood  of  those  portions  of  joints  that   have  undergone 

1  Marinesco. 


28 


GUY    HINSDALE,    M.D. 


Fig.  i; 


impairment  of  innervation.  The  modus  operandi,  according  to  Marinesco 
and  others,  is,  therefore,  a  mechanism  which,  starting  in  the  centripetal 
nerves  of  the  articulation,  reacts  in  such  a  way  upon  the  vasomotor  centres, 
and  thence  again  to  the  vasomotor  fibres  distributed  to  the  articular  sur- 
faces, that  the  trophic  changes  result. 

To  sum  up  the  determination  of  the  two  forms  of  arthropathy  as  ob- 
served in  syringomyelia,  tabes,  etc.,  we  may  say  that  if  there  exists  only  an 
impaired  action  of  the  sensory  nerves,  by  which  they  are  incompetent  to 
transmit  impressions  from  the  joint  to  the  centre,  the  atrophic  form  of 
arthropathy  will  result.  If  now  there  is  added  a  compensatory  adjustment 
by  which  fibres  remaining  intact  bring  about  an  increase  of  nutrition  to  the 
surrounding  unaffected  portions  of  the  articulation,  we  will  have  the  phe- 
nomena of  hypertrophy. 

Attention  is  drawn  to  the  influence  of  pathogenic  microbes  in  the  pro- 
duction of  arthropathies.  Where  innervation  is  impaired  the  tissues,  par- 
ticularly at  the  extremities,  are  not  well  able  to  resist  the  invasion  of  microbes. 
Such  affected  areas  constitute  the  points  of  least  resistance,  where  their  pene- 
tration is  easy  and  their  multiplication  undisturbed.  Those  changes  of 
infectious  nature  are  well  seen  in  Morvan's  type  of  syringomyelia,  and  in 

a  case  of  combined  syringomyelia  and 
leprosy, — such  as,  for  instance,  one 
reported  by  Souza-Martin.  As  in  the 
arthropathy  of  hemiplegia,  so  in  Mor- 
van's type  of  syringomyelia,  the  changes 
are  due  to  the  combined  influence  of 
a  direct  pathological  process  involving 
the  central  nervous  system  and,  in  ad- 
dition, the  action  of  pathogenic  mi- 
crobes which  have  been  introduced  from 
without  at  a  vulnerable  point. 

We  have  referred  to  the  resemblance 
which  the  hypertrophic  arthropathy  of 
syringomyelia  may  bear  to  arthritis  de- 
formans. Volkmann  endeavored  to 
make  the  anatomical  distinction  in  these 
cases  that  in  the  latter  disease  the  for- 
mation of  new  bone  is  confined  to  the 
interior  of  the  joint  capsule,  while  in 
the  spinal  arthropathies  there  may  be 
extensive  ossification  of  the  periarticular 
soft  parts  with  formation  of  osteophytes. 
Such  a  distinction,  however,  does  not  hold,  for  examples  of  arthritis  de- 
formans are  met  with  on  post-mortem  examination  in  which  there  were 
abundant  bony  formations  outside  the  limits  of  the  affected  joint,  and 
especially  in  the  adjacent  tendons  and  ligaments.     The  articular  surfaces 


Arthropathy  of   Morvan's    type 
mann's  case.) 


(Cursch- 


SYRINGOMYELIA. 


29 


co-ossified  in    places   may  be  deformed  either  by  partial  fractures  or  by 
osteophytes  with  which  they  are  surrounded.     Isolated  bony  growths,  de- 


veloped in  the  tendons  or  aponeuroses,  seem   to  be  met  with   more  often  in 
syringomyelia  than  in  tabes.1 

In   the  hypertrophic  form   the  ligaments  and   the  capsule  of  the  joints 


1   For  example,  in  a  ease  of  1 1  oilman  n's,  of  syringomyelic  arthropathy,  there  was 
an  osteoma  of  the  anconeus  mu 


30 


GUY    HINSDALE,    M.D. 


Fir;.  19. 


involved  are  relaxed  or  destroyed,  with  a  consequent  mobility  of  the  adja- 
cent ends  of  the  bone.  Such  was  the  condition  in  a  patient  of  Dr.  Alexis 
Thomson,  of  Edinburgh.  (Fig.  ]5.)  A  similar  condition  was  also  seen  in 
Dr.  Dercum's  case  at  the  Philadelphia  Hospital.  (Fig.  18.)  Dr.  Thomson 
calls  attention  to  the  fact  that  it  is  clearly  the  duty  of  the  surgeon  in  all 
cases  of  unusual  forms  of  joint-disease,  repeated  dislocation,  or  spontaneous 
fracture,  to  investigate  accurately  the  sensibility  to  pain  and  temperature, — 
features  which  will  occupy  our  attention  later, — for  otherwise  this  disease 
will  continue  to  escape  recognition  in  surgical  practice. 

(d)  The  Bones. — Lastly,  we  may  have  serious  alterations  of  the  shafts 
of  the  bones.  Fractures  occasionally  occur  spontaneously,  or  by  slight 
efforts  or  accidents.  These  fractures,  like  the  arthropathies,  are  painless, 
and  hence  may  escape  detection  for  a  considerable  length  of  time.     Union 

is  delayed,  and  there  is  a  great  liability  to 
vicious  or  redundant  callus.  In  some  cases 
the  fracture  remains  ununited,  and  a  false 
joint  forms.  One  of  the  best  illustrations  of 
fractures  of  this  kind  is  that  of  Schultze, . 
cited  by  Thomson  and  Bruhl.  It  occurred 
in  a  healthy  man,  aged  twenty-four,  in  whom 
the  first  evidence  of  syringomyelia  was  a 
"spontaneous"  fracture  of  the  humerus, 
caused  by  an  energetic  muscular  effort.  Be- 
cause of  the  loss  of  sensibility  to  pain  this 
patient  only  knew  of  his  fracture  by  the 
noise  of  the  break  and  by  the  loss  of  power 
in  the  limb.  He  subsequently  fractured  his 
left  radius  and  fifth  metacarpal, — all  bones 
of  the  upper  extremity.  After  death,  at  a 
later  period,  of  septic  meningitis,  Schultze 
found  that  all  the  fractures  had  united  in  a 
satisfactory  manner,  and  that  there  was  no 
abnormal  fragility  of  the  bones,  such  as  might 
have  been  reasonably  expected.  He  en- 
deavors to  explain  the  liability  to  fracture 
in  these  cases  by  the  loss  of  the  muscular 
sense  and  of  sensibility  to  pain,  allowiug  the 
patient  to  exert  more  muscular  effort  than  is 
required  for  the  object  in  view  or  than  the  bone  can  stand. 

Lastly  we  may  have  trophic  changes  in  the  bones,  particularly  of  the 
hands  and  fingers,  that  partake  of  the  nature  of  acromegaly.1 

(2)  Deviations  of  the  Spinal  Column. — Changes  in  the  spinal  column 
have  been  observed  in  so  many  cases  of  syringomyelia  that  they  have  come 


Scoliosis  in  syringomyelia.     (Cursch 
mann's  case.) 


1  See  cases  of  Marie,  Holsckevnikoff,  and  Peterson. 


SYRINGOMYELIA.  .°>1 

to  be  regarded  as  a  characteristic  symptom.  Lancereaux  was  probably  the 
first  to  notice  this  in  a  case  of  syringomyelia,  which  he  described  in  1861 
under  the  name  of  hypertrophy  of  the  ependyma.  Although  the  earlier 
observations  on  syringomyelia  generally  made  no  mention  of  the  state  of 
the  spine,  it  is  now  given  a  prominent  place  in  the  symptomatology  of  the 
disease.  In  an  analysis  of  the  one  hundred  and  eighteen  cases  found  in 
the  appendix,  we  find  that  deviations  of  the  spinal  column  are  noted  in 
forty-four  cases.  Bruhl  states  that  this  frequency  is  about  fifty  per  cent, 
and  Sehlesinger  gives  forty  per  cent.  The  more  carefully  the  examination 
is  made  the  more  likely  will  the  percentage  be  found  to  be  increased.  The 
accompanying  photograph  of  one  of  Curschmann's  cases  shows  this  deform- 
ity in  a  marked  degree.  In  one  of  the  cases  described  by  the  author  (case 
of  Robert  Collins,  see  Case  No.  I.)1  there  is  a  marked  deformity.  Hallion, 
Hoffmann,  and  Jeffries  have  also  published  excellent  examples. 

The  usual  form  of  deviation  is  scoliosis;  in  some  cases  this  is  associated 
with  kyphosis.  Pure  kyphosis  is  very  rare,  but  has  been  observed  in  the 
cervical  region.  Lordosis  is  uncommon,  but  when  present  may  be  looked 
for  in  the  lumbar  region. 

Scoliosis  may  involve,  together  with  the  compensatory  curves,  the  entire 
length  of  the  spinal  column,  but  the  favorite  seat  is  the  dorsal  region.  The 
convexity  of  the  curve  looks  usually  to  the  side  which  is  affected  earliest 
and  on  which  the  muscles  are  impaired.  This  impairment  allows  the  stronger 
muscles  of  the  opposite  side  to  contract  more  effectually,  with  the  result 
that  a  convexity  on  the  opposite  side  of  the  spinal  column  is  produced. 
This  deformity,  obviously,  is  more  marked  in  cases  where  the  disease  is 
unilateral. 

Exceptions  to  this  may  occur,  as,  for  instance,  in  a  case  of  Kahler's  in 
which  the  spine  was  normal,  although  there  was  a  strong  predominance  of 
the  disease  on  the  left  side;  but  in  this  case  the  muscles  of  the  trunk  were 
believed  to  be  spared. 

In  one  hundred  and  eighteen  cases  analyzed  in  appendix,  scoliosis  was 
noted  in  thirty-six. 

Convexity  to  right 13 

.Muscular  defects  began  in  right 10 

Muscular  defects  began  in  left 2 

Convexity  to  left 8 

Muscular  defects  began  in  right 2 

Muscular  defects  began  in  left 3 

Although  there  may  be  considerable  difference  in  the  height  of  the 
shoulders,  immobilization  of  the  corresponding  part  of  the  spine  and  other 
evidences  of  deformity,  there  is,  as  a  rule,  no  special  pain  or  discomfort. 
Should  pain  exist  in  an  exceptional  case  there  is  no  evidence  that  it  is  due 
to  a  meningitis.     There  may,    however,  be  a  certain   degree  of  pain   on 

'See  Cases  XXVII.,  XXXIV.,  MAX. 


32  GUY    HINSDALE,    M.D. 

pressure  with  stiffness  of  the  affected  portion  of  the  spinal  column.  This 
may  vary  as  to  the  time  at  which  it  is  apparent,  either  early  or  late  in  the 
history  of  the  affection.  The  curvature  itself  may  be  coincident  with  the 
earliest  symptoms,  but  ordinarily  it  is  apparent  several  years  after  the  on- 
set of  the  disease.  In  cases,  such  as  one  published  by  Bruhl,  where  the 
scoliosis  was  observed  at  the  age  of  sixteen  and  a  half  years,  but  where  the 
disease  did  not  commence  to  be  marked  until  the  thirty-third  year,  we  may 
fairly  question  the  relationship  of  the  two.  It  is  not  possible  in  most  cases 
to  state  the  exact  time  at  which  the  deviation  occurred,  since  no  pain  is 
present  and  as  it  is  not  ordinarily  noticed  until  actual  deformity  appears. 

The  nature  of  deviation  of  the  vertebral  column  as  observed  in 
syringomyelia  has  given  rise  to  various  opinions.  Roth  believes  that 
scoliosis  is  of  muscular  origin,  arising  from  an  atrophy  of  the  "muscles 
transversaire  epineux,"  which  may  exist  early  in  the  case.  We  have  noted 
in  a  study  of  cases  given  in  the  appendix  that  atrophy  of  the  trapezius 
(cucullaris)  is  rather  frequently  noted.  The  origin  of  this  muscle  embraces 
the  entire  extent  of  the  spinal  column  above  the  first  lumbar  vertebra,  and 
it  can  readily  be  understood  how  atrophy  of  it  or  of  any  considerable  por- 
tion of  its  fibres  may  affect  the  direction  of  the  spine. 

It  is  quite  probable  that  the  muscles  are  not  alone  in  their  influence  in 
causing  deviation  of  the  spine  in  this  disease.  The  tendency  to  affections 
of  the  joints  and  of  the  long  bones  in  syringomyelia  would  suggest  that 
the  vertebras  and  their  articulations  may  share  the  trophic  change,  which  is 
more  evident  in  other  localities,  so  that  we  may  hold,  in  view  of  the  facts 
that  have  been  presented,  that  the  scolioses  or  the  more  pronounced  de- 
formities are  evidences  of  trophic  disorder  dependent  on  the  changes  in  the 
gray  matter  of  the  cord.  In  this  respect  we  see  in  it  a  strong  analogy  to 
the  spinal  deviation  observed  in  Friedreich's  ataxia. 

(3)  Vasomotor  Disturbances. — These  changes  are  commonly  observed  and 
give  rise  in  some  cases  to  considerable  distress.  The  superficial  circulation 
in  the  affected  areas  is  disturbed,  being  either  inadequate  to  proper  bodily 
comfort  or,  on  the  other  hand,  by  its  excess  giving  rise  to  redness,  swelling, 
and  actual  elevation  of  the  local  temperature.  In  the  first  instance  a 
sluggish  circulation  is  naturally  attended  with  a  chilling  of  the  part  and  a 
cyanotic  appearance  of  the  extremity  involved.  The  surface  temperature  is 
lowered  and  the  patient  may  complain  of  a  sense  of  cold.  Subjective  sen- 
sations of  cold  in  cases  where  no  objective  symptoms  are  apparent  are  com- 
mon, and  in  many  cases  these  feelings  are  distributed  over  a  large  area, 
The  patient  complains  of  coldness  of  a  limb  or  of  a  sense  of  cold  water 
running  down  the  back.  On  the  other  hand,  the  sensation  may  be  of  burn- 
ing or  smarting  and  may  vary  very  much  even  in  the  same  individual. 

The  skin  itself  quickly  responds  to  external  stimuli,  so  that  a  slight 
stroke  along  the  skin  of  the  back  will  leave  a  reddish  line,  which  persists 
for  some  time  after  the  stimulus  has  been  applied.  This  feature  is  common 
in  spinal  disease  under  the  name  of   dermographism  or  "homme  auto- 


SYRINGOMYELIA.  33 

graphique,"  and  is  therefore  of  diagnostic  value  only  when  taken  in  con- 
nection with  other  more  characteristic  symptoms.  So  also  cedernas  are 
noted  in  this  disease  and  are  distinctly  of  nervous  origin.  They  are  ob- 
served, when  present,  on  the  dorsum  of  the  hand  or  in  the  lower  part  of 
the  forearm.  The  "tumeurs  pateuses"  observed  by  Roth  are  doubtless  of 
this  nature. 

Disturbances  of  the  secretion  of  sweat  are  quite  commonly  observed, 
excessive  in  some  regions  while  suppressed  in  others.  The  excess  is  gen- 
erally observed  in  the  anaesthetic  areas.  French  writers,  including  Dejerine, 
Grasset,  and  Bruhl,  and  Schultze  and  Fiirstner  and  Zacher,  in  Germany, 
have  made  interesting  observations  on  this  point. 

(4)  Disorder  of  the  Sphincters. — These  are  rarely  disturbed. 

In  the  first  case  summarized  in  our  appendix,  that  of  Abbe  and  Coley, 
there  was  partial  loss  of  control  of  the  bladder  and  rectum,  and  before  death 
a  violent  cystitis  ensued.  In  a  case  of  Charcot's  death  was  caused  by  a 
spontaneous  perforation  of  the  bladder  following  a  simple  ulcer.  In  a  case 
of  Oppenheim's  also  death  was  due  to  bed-sores  and  cystitis. 

Incontinence  of  the  bowels  is  rare  but  constipation  is  commonly  noted. 
In  Preobrajensky's  case  (No.  LXXIX.)  there  were  retention  of  urine  and 
incontinence  of  fasces;  death  occurred  in  the  course  of  three  weeks  from 
pyelonephritis  and  purulent  cystitis. 

In  traumatic  cases,  where  great  violence  is  done  to  the  cord  with  accom- 
panying paraplegia,  we  naturally  look  for  incontinence  of  fasces  and  retention 
of  urine.  In  Schlesinger's  recently  published  case  (No.  XIV.,  Monograph, 
1895)  the  above  symptoms  were  present  as  a  result  of  luxation  of  the  twelfth 
dorsai  vertebra  with  compression  of  the  cord.  At  the  autopsy,  three  months 
later,  a  dilatation  of  the  central  canal  was  found  throughout  the  entire  dor- 
sal cord  above  the  point  of  luxation.  Cystitis  and  pyelonephritis  were  also 
present. 

(5)  Ocular  Symptoms. — The  disturbances  of  the  eyes  in  syringomyelia 
may  be  properly  considered  under  a  separate  heading,  although  they  are 
closely  related  to  the  bulbar  symptoms  which  will  be  more  fully  considered 
later. 

Pupils. — Inequality  of  the  pupils  is  not  an  uncommon  symptom.  In 
the  one  hundred  and  eighteen  cases  found  in  the  appendix  we  find  this  noted 
twenty-seven  times.  (Cases  III.,  V.  X.,  XVII.,  XXVL,  XXVII., 
XXXV.,  XXXVI.,  XLI.,  XLU.,  XLIII.,  XLIV.,XLVL,  XL1  X  . 
LVIII.,  LXIII.,  LXIV.,  LXXII.,  LXXIII.,  LXXVI.,  XCL,  C,  CV. 
CXIII,  CXVL, CXVIII.) 

In  eighteen  cases  the  right  pupil  was  the  larger;  in  six  cases  the  left. 
Bruhl  records  tins  symptom  ten  times  in  thirty-six  cases  and  Schlesinger 
twenty-four  times  in  two  hundred  cases  in  all  the  literature  accessible.  By 
adding  the  cases  of  inequality  of  the  pupils  due  to  paralysis  of  the  sympa- 
thetic the  proportion  rises  to  twenty-five  per  cent.  Paralysis  of  the  sym- 
pathetic nerve  may  occur  from  lesion  of  the  cord  in  the  upper  dorsal  region; 


34 


GUY    HINSDALE,    M.D. 


it  is  generally  unilateral,  but  bilateral  paralyses  have  been  recorded  by 
Schlesinger,  who  remarks  that  it  is  one  of  the  initial  symptoms  of  syringo- 
myelia, particularly  of  the  cervical  type  and  those  that  are  accompanied  by 
marked  muscular  atrophy.  The  pupils  in  almost  every  case  observed  re- 
acted to  both  light  and  accommodation.  In  case  No.  LXXII.  which  we 
report  convergence  to  light  was  absent.  Immobility  of  the  pupils  with 
inequality  is  noted  in  a  very  few  cases  of  syringomyelia  as  well  as  tumors 
of  the  spinal  cord.  The  case  of  Oppenheim  (G.  P.1)  is  an  example,  and 
other  cases  have  been  recorded  by  Glaser,  Schultze,  Homen  (q.  v.),  Brut- 
tan,  and  Tornow. 

Nystagmus  is  not  an  unusual  symptom.  We  find  that  it  is  noted  fifteen 
times  in  one  hundred  and  eighteen  cases,  and  is  usually  horizontal,  but  may 
be  vertical  or  diagonal.  It  is  one  of  the  earlier  symptoms,  and  is  indicative 
of  lack  of  muscular  tone  and  co-ordination  of  the  motor  apparatus  of  the  eye. 
In  this  respect  it  is  entirely  comparable  with  the  nystagmus  of  Friedreich's 
disease. 

The  visual  fields  are  occasionally  narrowed.  This  was  noted  in  the  case 
of  two  men  in  a  total  of  seventy-three  men,  and  in  five  women  in  a  total  of 
thirty-eight  women.  French  authors  believe  that  this  symptom  is  confined 
to  cases  complicated  with  hysteria,  but  this  statement  may  fairly  be  ques- 
tioned.    The  two  cases  which  have  been  reported  by  Eskridge  have  been 

Fig.  20. 


280  260  280 ' 260 

Contraction  of  the  color-fields  in  a  case  of  syringomyelia. 

very  carefully  studied  in  this  respect,  and  both  showed  narrowing  of  the 
visual  fields.  Neither  of  these  could  be  construed  as  hysterical.  Espe- 
cially in  the  case  of  one  of  them  (George  S.)  was  this  considered  and  ruled 
out.  On  roughly  testing  the  eyes  there  was  "  an  apparent  approach  to  left 
lateral  homonymous  hemianopsia,"  but  by  repeated  careful  tests  with  the 


1  Archiv  fur  Psychiatrie,  1893,  p.  324. 


SYRINGOMYELIA.  35 

aid  of  the  perimeter  (see  accompanying  figure)  it  will  be  seen  that  while 
all  fields  are  lessened,  the  left  eye  showing  the  greatest  contraction,  there 
is  not  a  condition  of  hemianopsia.  Two  examinations  were  made  thirty- 
nine  days  apart.  Schlesinger  cites  twenty  cases  occurring  in  more  hys- 
terical subjects  where  there  was  narrowing  of  the  visual  fields  and  sixty- 
seven  cases  where  the  fields  were  definitely  known  to  be  normal.  When 
narrowing  does  occur  it  is  found  chiefly  in  the  color  fields,  particularly 
green.  Scotoma  has  not  been  observed.  The  condition  of  the  external 
ocular  muscles  is  not  commented  on  excepting  in  very  few  cases.  In  these 
convergent  strabismus  from  early  childhood  was  noted  six  times.  (Cases 
XXXIIL,  XL.,  LIV.,  LXVIL,  LXXX.,  CXI.) 

The  ophthalmoscopic  appearances  when  mentioned  are  usually  negative. 

In  Eskridge's  second  case,  that  of  Jesse  C.  (No.  XVIII.),  the  disk  of 
the  right  eye  was  of  a  grayish-white  color,  with  a  central  physiological  cup ; 
its  edge  was  sharp ;  the  sclerotic  ring  was  seen  around  the  disk  rather  more 
clearly  on  the  temporal  than  on  the  nasal  side.  Two  small  pigmeut  deposits 
were  seen  in  the  upper  inner  quadrant  of  the  fundus  about  the  diameter  of 
the  disk  from  its  margin.  The  fundus  of  the  left  eye  presented  very  much 
the  same  picture  as  that  of  the  right,  both  having  the  appearance  of  com- 
mencing gray  atrophy.  The  color-fields  of  these  eyes  are  published  in 
"  International  Clinics,"  3d  Series,  vol.  iv.  p.  135. 

In  rare  cases  amblyopia  or  even  amaurosis  from  atrophy  of  the  optic 
nerves  has  been  recorded.1 

(6)  Bulbar  Symptoms. — The  invasion  of  the  medulla  oblongata  by  the 
glioma  or  by  the  formation  of  a  cavity  gives  rise  to  a  distinct  train  of  symp- 
toms. Among  these  laryngeal  palsies  assume  a  prominent  place.  Sensory 
paralysis  of  the  larynx  is  somewhat  uncommon,  but  motor  paralysis  is  the 
form  more  frequently  observed.  The  motor  derangement  consists  more 
frequently  in  interference  with  phonation  than  in  disturbances  of  respiration. 
Unilateral  paralysis  of  the  recurrent  laryngeal  branch  of  the  pneumogastric 
is  the  commonest  form  observed.  The  paralysis  is  usually  unilateral  but 
in  exceptional  cases  may  be  bilateral. 

Where  bulbar  involvement  is  marked  we  have  more  extended  paralysis 
of  motion.  The  muscles  of  the  pharynx,  the  tongue,  the  lips,  and  even  the 
facial  muscles  may  be  involved.  It  thus  happens  in  a  well-marked  case 
that  the  expression  of  the  face  is  altered,  owing  to  paralysis  of  motor 
branches  of  the  trigeminus.  The  lips  are  unable  to  perform  the  act  of  suc- 
tion, prehension  ;  the  patient  is  unable  to  whistle.  Mastication  is  interfered 
with  and  solid  food  requires  to  be  washed  down  with  water;  saliva  becomes 
unmanageable  owing  to  the  difficulty  in  swallowing  it.  The  motions  of  the 
tongue  are  impaired  and  its  structure  undergoes  atrophy  on  one  or  both 
sides, — speech  is  thick. 

1  See  casts  recorded  by  Simon,  Schultze,  Westphal,  Furatner  and  Zacher,  Eick- 
holt,  Glaser,  and  Schuele. 

3 


36  GUY    HINSDALE,    M.D. 

Sensory  changes,  if  sought  for,  will  be  found,  in  a  typical  case,  to  be 
present  within  the  mouth,  the  throat,  and  the  larynx,  as  well  as  the  external 
portions  of  the  body.  In  a  case  carefully  studied  by  S.  Solis-Cohen  all  the 
foregoing  symptoms  were  found,  and  extensive  sensory  changes  as  well. 
While  tactile  sensation  was  almost  perfectly  preserved,  it  was  found  that  at 
times  there  were  places  on  the  face,  lips,  and  within  the  throat  where  it 
seemed  blunted.  The  temperature  sense  was  found  to  be  both  blunted  and 
perverted  on  the  right  side  of  the  face,  while  at  the  base  of  the  tongue, 
in  the  oesophagus  and  the  larynx,  it  was  blunted  but  not  lost.  Taste  was 
absent  from  the  anterior  portion  of  the  tongue  in  the  distribution  of  the 
gustatory  branch  of  the  nerve. 

Other  bulbar  symptoms,  such  as  vertigo,  attacks  of  transient  blindness, 
etc.,  may  be  noted,  as  has  been  recorded  in  the  case  referred  to. 

Laryngeal  symptoms  are  generally  gradual  in  their  onset  and  pursue  a 
chronic  course.  Should,  however,  bulbar  manifestations  occur  suddenly  by 
apoplectiform  attacks  they  would  probably  be  of  a  hemorrhagic  nature,  and 
would  be  accompanied  by  vertigo,  clouding  of  the  mind,  and  even  complete 
loss  of  consciousness,  possibly  with  vomiting.  This  symptom  might  mark 
the  extension  of  the  glioma  into  the  brain  if  accompanied  with  severe  head- 
ache. Disturbances  of  hearing,  of  central  origin,  and  the  occasional  appear- 
ance of  polyuria  may  be  added  to  this  group  of  symptoms.1 

3.  Symptoms  of  Posterior  Poliomyelitis. — Degeneration  or  excavation  of 
the  posterior  horns  of  the  cord  gives  rise  to  the  most  characteristic  symp- 
toms of  syringomyelia.  Disturbances  of  sensation  are  among  the  earliest 
features  which  can  be  traced  in  the  history  of  most  cases,  and  careful  inquiry 
will  almost  always  reveal  incidents  depending  on  the  loss  of  pain  sense  or 
heat  sense  that  antedate  by  several  years  the  symptoms  which  lead  a  pa- 
tient to  consult  a  physician.  But  sensory  disturbances  are  not  always  ap- 
parent. There  are  exceptional  cases  in  which  such  unusual  variations  from 
the  classical  type  have  been  present  that  the  most  accomplished  clinicians 
have  been  led  into  error.  It  was  just  in  this  respect  that  Raymond  was 
led  into  a  mistaken  diagnosis  of  a  case,  for  it  was  only  during  the  last 
fifteen  months  of  the  patient's  life  that  any  sensory  changes  were  found 
although  carefully  searched  for.  Rare  cases  of  this  kind,  in  which  during 
the  entire  course  of  the  disease  no  sensory  changes  have  been  noted,  are 
recorded  by  Schuele,  Schiiltze,  Krauss,  Striimpell,  Bernhardt,  and  Par- 
men  tier. 

In  a  case  recently  reported  by  Schlesinger  (Case  VI.,  Monograph,  1895), 
a  woman,  aged  thirty-nine  years,  presented  no  loss  of  sensation  in  any  form. 


1  See  articles  by  Herman  F.  MUller,  A.  Raichline,  S.  Solis-Cohen,  H.  Schlesinger, 
Klebs,  Krauss,  Grasset,  and  Adolf  Schmidt. 

The  author  would  also  call  attention  to  the  extraordinary  statement  by  Dr.  Fred- 
erick I.  Roberts  (Theory  and  Practice  of  Medicine,  Ninth  Edition,  1894,  p.  1108) 
that  there  is  no  bulbar  involvement  in  syringomyelia. 


SYRINGOMYELIA.  37 

The  pressure  sense,  localization  sense,  pain  sense,  and  temperature  sense, 
for  both  warm  and  cold,  were  normal ;  there  was,  however,  hyperesthesia 
and  hyperalgesia.  The  clinical  diagnosis  of  syringomyelia  was  made  by 
both  Schlesinger  and  Ewald  on  the  strength  of  other  symptoms.  Death 
followed  a  surgical  operation,  and  a  cavity  extending  from  the  lumbar 
region  throughout  the  entire  dorsal  and  cervical  regions  was  demonstrated 
at  the  autopsy. 

The  forms  of  anaesthesia  which  require  investigation  in  a  suspected  case 
of  syringomyelia  are  as  follows: 

Thermo-anaesthesia  (almost  invariably  present). 

Analgesia  (generally  present). 

Tactile  anaesthesia  (rarely  present). 

Loss  of  muscular  sense  (rare). 

Loss  of  pressure  sense  (rare). 

Loss  of  localization  sense  (rare). 

It  is  quite  unusual  to  find  present  in  any  given  case  thermo-anaesthesia, 
analgesia,  and  tactile  anaesthesia,  a  condition  conveniently  expressed  as 
triple  anaesthesia.  The  symptom  complex,  which  is  considered  almost 
pathognomonic  of  the  disease,  is  a  combination  of  thermo-anaesthesia  and 
analgesia  with  preservation  of  tactile  sensation.  This  constitutes  the  famous 
"  dissociation  symptom,"  as  Charcot  has  designated  it. 

This  dissociation  of  sensibility  is  not  confined,  however,  to  syringo- 
myelia ;  it  is  found  in  the  case  of  several  affections  of  the  nerve-centres, 
very  frequently,  for  example,  in  cervical  pachymeningitis;  occasionallv  in 
neuritis,  hysteria,  alcoholic  neuritis,  traumatic  neuritis,  leprosy,  haemato- 
myelia,  locomotor  ataxia,  and  extramedullary  tumor  of  the  cord  ;  and  in 
mixed  cases  where  there  is  injury  both  to  the  cord  and  to  the  nerve-roots. 
Two  cases  illustrative  of  the  latter  condition,  in  which  the  dissociation 
symptom  was  well  marked,  have  been  recently  published  by  Lloyd,  under 
the  title  of  "Traumatic  Affections  of  the  Spinal  Cord  simulating  Syringo- 
myelia." '  In  the  first  of  these  cases  a  man,  in  falling  from  a  scaffold, 
struck  the  back  of  his  neck,  and  was  believed  to  have  sustained  a  fracture 
of  the  spinal  column.  The  entire  body,  including  both  arms  and  legs,  was 
paralyzed.  He  recovered  from  this,  and  eight  years  later  he  fell  again  and 
struck  the  back  of  his  head  and  spine  between  the  shoulders.  Partial  re- 
covery took  place,  but  an  examination  ten  years  afterwards  revealed  to  some 
extent  the  dissociation  symptom.  There  was  anaesthesia  to  cold  ;  cold  objects 
in  the  affected  area,  as  shown  in  the  charts  (Figs.  2  and  3,  loc.  cit.),  were 
called  hot.  Analgesia  of  the  right  side  was  present,  while  tactile  sensi- 
bility was  everywhere  good. 

In  a  second  case  a  laborer,  at  the  age  of  thirty,  injured  his  cervical 
and  dorsal  spine  by  having  fallen  into  a  canal  and  being  jammed  be- 
tween  two  canal-boats,  and  was  unable   to   resume  work    for   three  months. 


Journal  of  Nervous  and  Mental  Disease,  June,  1894. 


38 


GUY    HINSDALE,    M.D. 


At  the  age  of  fifty-seven  he  was  severely  injured  by  a  fall  of  a  bank  of 
earth.  After  twenty-four  hours'  unconsciousness  he  was  found  to  be  paral- 
yzed in  the  left  arm  and  leg.  Three  years  later  an  examination  showed, 
in  addition  to  angular  deformity  of  the  spine,  atrophy  and  fibrillary  con- 
tractions of  the  left  shoulder  girdle  muscles,  a  noteworthy  disorder  of  sen- 
sation. (See  Figs.  5  and  6,  loc.  cit.)  The  patient  was  unable  to  distinguish 
heat  fronfcold  or  to  recognize  either  in  the  region  marked  on  the  chart.    The 

Fig.  21. 


Aricsst/iesta 


Thermo 
Ancestkesca. 


Aricpsthesca. 


T/zer/nc 


Syringomyelia.— Showing  segmental  distribution  of  sensory  symptoms. 

thermo-amesthesia  was  on  the  right  side,  the  side  opposite  the  paralysis  of 
motion.  There  was  an  area  of  tactile  anaesthesia  (not  portrayed  on  the  chart) 
involving  the  right  leg. 

It  may  be  possible  that  in  these  cases  where  trauma  has  played  such  a 
conspicuous  part  the  conditions  may  be  explained  by  the  subsequent  dis- 
covery of  hsematomyelia  and  consequent  excavation,  the"  myelite  cavitaire" 
of  French  authors.  However  this  may  be,  this  author  did  not  feel  justified 
in  making  a  diagnosis  of  syringomyelia,  in  these  cases  at  least,  in  the  present 


SYRINGOMYELIA. 


39 


stage  of  their  clinical  manifestations.     On  the  other  hand,  it  is  quite  likely 
that  in  less  careful  hands  a  positive  diagnosis  would  be  claimed.1 

Thermo- Ansesthesia. — Loss  of  power  to  recognize  heat  and  cold  is  prob- 
ably one  of  the  earliest  symptoms  ;  it  is  a  prominent  feature  all  through  the 


Fig.  22. 


Ancesthesca 


Anesthesia. 


Thermo 
Ancesh'iestci . 


Syringomyelia.— Showing  segmental  distribution  of  sensory  symptoms. 


history  of  the  majority  of  cases,  although  varying  considerably  in  its  extent 
and  in  its  degree  in  individual  instances.  It  is  most  commonly  found  in 
the  hands  and  fingers  of  one  side,  or  it  may  extend  throughout  one  or  both 
upper  extremities,  or  be  in  a  measure  present  throughout  almost  the  entire 
area  of  the  body.  Thermo-ansesthesia  is  commonly  limited  by  the  median 
line  of  the  body,  and  in  these  cases  where  both  upper  and  lower  quadrants 
are  involved  is  sometimes  described  as  hemiplegic  thermo-ansesthesia. 

The  line  of  demarcation  between  the  normal  and  abnormal  area  is  gen- 


1  See,  also,  u  publication  by  R.  Verhoogen,  entitled  "  Dissociation  de  la  Sensi- 
bility dans  un  Cas  de  Lesion  des  Nerfs  du  Plexus  brachial."     Brussels,  L894. 


40  GUY    HINSDALE,    M.D. 

erally  quite  sharply  drawn  ;  particularly  is  this  the  case  on  crossing  the 
median  line  from  the  affected  to  the  unaffected  side. 

In  its  distribution,  thermo-ansesthesia  sometimes  involves  the  face  (as- 
cending branch  of  the  fifth  nerve);  more  often  it  affects  the  sides  and  back 
of  the  neck  and  is  likely  to  be  limited  by  the  hair  of  the  scalp  behind 
(distribution  of  the  occipitalis  major  and  minor).  It  is  obviously  more 
likely  to  be  discovered  in  the  exposed  areas  of  the  skin,  but  on  careful 
exploration  areas  on  the  thorax,  horizontal  belts  in  the  abdomen,  or  possibly 
areas  in  the  outer  aspects  of  the  thighs  maybe  discovered.  Charcot  asso- 
ciates its  distribution  rather  oddly  with  the  names  of  garments  for  the 
various  localities ;  thus  he  makes  out  the  "  forme  de  gant,  de  manchette,  de 
manche,  de  bas,  de  culotte,  de  jambe  de  pantelon,  de  petite  veste,"  etc. 
The  distribution  is  sometimes  symmetrical ;  it  is  usually  progressive  in 
character. 

To  elicit  information  in  a  suspected  case  of  thermo-ansesthesia  it  is  cus- 
tomary to  use  two  test-tubes  of  precisely  similar  form  and  appearance,  one 
containing  hot  water  and  the  other  cold.  It  is  preferable  to  use  a  small 
object  like  a  test-tube  instead  of  a  more  bulky  bottle,  for  the  reason  that 
normal  skin  areas  adjacent  to  the  affected  regions  may  be  sensible  to  radia- 
tion of  heat  from  a  larger  mass.  The  wide  difference  of  temperature 
present  in  the  tubes  at  the  start  tends  to  grow  smaller  as  the  examination 
progresses  unless  precautions  are  taken.  It  is  therefore  desirable  to  know, 
by  using  a  thermometer,  the  exact  temperatures  of  the  testing  apparatus. 
Charcot  used  a  surface  thermometer,  the  bulb  of  which  was  inclosed  in  a 
metallic  cylinder  filled  with  copper  filings.  By  these  means  the  temperature 
acquired  on  placing  the  instrument  over  an  alcohol-lamp  may  be  maintained 
for  a  considerable  time.  (See  also  article  by  Leegaard.)  Glass  balls  pro- 
vided with  a  perforated  cork  for  the  passage  of  a  thermometer  and  half  filled 
with  water  may  be  used. 

The  glass  ball  can  readily  be  heated  in  an  alcohol  flame  as  far  as  212°  F. 
Great  care  should  be  used  in  tests  with  temperatures  above  180°  F.,  as  too 
long  a  contact  might  produce  burns,  the  healing  of  which  would  be  trouble- 
some. 

Thermo-ansesthesia  may  be  said  to  be  complete  when  the  patient  fails  to 
recognize  either  ice  when  placed  on  the  skin  or  an  object  heated  to  near  the 
boiling  point.  Such  extreme  loss  of  temperature  sense  is  not  commonly 
met  with,  and  the  recognition  of  intermediate  grades  becomes  necessary  in 
most  cases.  Any  one  who  fails  to  distinguish  differences  of  5°  C.  or  9°  F. 
may  be  gaid  to  have  thermo-ansesthesia  (Roth).  There  is  need  in  difficult 
or  doubtful  cases  to  make  numerous  examinations  with  relatively  slight 
differences  of  temperature,  especially  in  the  moderate  ranges  between  80° 
and  140°  F. 

Normal  individuals  vary  very  greatly  in  their  acuity  of  perception,  and 
the  time  reaction  varies  in  different  cases.  So  also  allowances  must  be  made 
for  the  natural  variations  of  acuteness  of  sensation  in  various  parts  of  the 


SYRINGOMYELIA. 


41 


body.  According  to  Weber  and  Nothnagel,  .40°  C.  can  be  distinguished 
at  the  finger-tips  in  favorable  subjects;  such  fine  differentiation  is  wholly 
impossible  without  the  most  delicate  and  reliable  instruments,  and  would 
fail  in  persons  whose  perceptive  powers  are  normally  more  sluggish.  It  is 
also  shown  that  at  extreme  temperatures  at  either  end  of  the  scale  slight 
differences  are  not  so  readily  recognized  as  at  the  more  moderate  ranges. 
High  temperatures  may  be  recognized  simply  as  painful  if  test  is  made  in 


Fig.  23. 


yjt  \Analge5fa. 


Syringomyelia. — Showing  segmental  distribution  of  sensory  symptoms. 


the  back,  the  thorax,  etc.,  while  at  certain  sensitive  points,  as,  for  instance, 
the  finger-tips,  they  may  be  recognized  in  their  true  character.  In  other 
cases  the  sense  is  perverted,  giving  rise  to  hyperesthesia  or  complete  reversal 
of  the  sense  of  heat  and  cold.  In  one  of  Bruhl's  cases  the  skin  of  the 
right  half  of  the  thorax  was  sensitive  to  thermic  impression  in  an  exagger- 
ated manner. 

The  application  of  tests  of  various  degrees  of  cold  is  not  quite  so  easy 


42 


GUY    HINSDALE,    M.D. 


on  account  of  the  difficulty  in  securing  a  series  of  different  temperatures 
below  that  of  the  surrounding  air.  On  this  account  abnormalities  in  the 
sense  of  cold  are  doubtless  frequently  overlooked.  Error  in  the  estimation 
of  the  degree  of  thermo-anaesthesia  is  liable  to  happen  by  reason  of  daily, 
and,  it  has  been  suggested,  by  hourly  variations  in  the  areas  of  distribution 

Fig.  24. 


e$t 


Syringomyelia.— Showing  segmental  distribution  of  sensory  symptoms. 


and  in  the  intensity  of  sensation.  Such  cases  are  recorded,  and  serve  to 
explain  discrepancies  which  arise  in  clinical  studies. 

In  general  the  same  regions  that  are  insensitive  to  heat  are  also  insensitive 
to  cold,  but  one  area  is  not  always  exactly  superimposed  upon  the  other,  and 
this  fact  had  led  to  the  belief  in  the  probability  of  the  existence  of  special 
nerve  elements  for  the  transmission  of  the  sensations  of  heat  and  of  cold. 
Cases  are  cited  in  which  warm  objects  are  recognized  over  certain  areas, 
while  cold  objects  are  not  recognized  in  the  same  location. 

It  should  be  mentioned  in  connection  with  thermo-ansesthesia  that  the 


SYRINGOMYELIA.  43 

mucous  membrane  occasionally  is  involved  as  well  as  the  cutaneous  sur- 
face. 

Analgesia. — Loss  of  the  sense  of  pain  in  certain  areas  is  one  of  the 
cardinal  symptoms  of  syringomyelia.  In  its  distribution  it  occurs  in  general 
in  the  same  areas  as  in  the  case  of  thermo-anaesthesia.  (Figs.  23  and  24.) 
It  may  be  of  various  degrees  from  partial  to  absolute  loss  of  pain  sense. 
The  prick  of  a  pin  is  not  recognized  as  painful.  So  profound  is  the  anal- 
gesia in  some  cases  that  abscesses  have  been  opened  and  even  fingers  ampu- 
tated and  joints  excised  without  a  particle  of  pain.  As  we  have  previously 
mentioned,  fractures  may  occur  without  any  pain  being  felt.  On  the  other 
hand,  in  exceptional  cases  hyperesthesia  has  been  recorded  in  place  of  anal- 
gesia. Charcot  explains  this  by  conceiving  that  the  period  of  destruction 
of  the  nerve  elements  is  preceded  in  some  way  by  a  period  of  irritation. 
Hyperesthesia,  when  present,  is  more  likely  to  be  found  in  the  lower  ex- 
tremities. 

In  estimating  the  degree  of  analgesia  it  should  be  borne  in  mind  that 
individuals  of  the  same  class  at  different  times  vary  greatly  in  this  regard, 
and  still  more  noteworthy  is  the  difference  between  different  classes  of  sub- 
jects. The  subject  of  dermal  pain  has  been  investigated  by  Mr.  Griffing, 
of  Columbia  College,  New  York.  He  shows  that  in  kilogrammes  the 
required  amount  just  causing  pain  was  as  follows:1 

Kilogrammes. 

For  boys 4.8 

For  college  students 5.1 

For  law  students 7.8 

For  women 3.6 

II.  Extrinsic  Symptoms. — Symptoms  due  to 

1.  Sclerosis  of  the  lateral  columns. 

2.  Sclerosis  of  the  posterior  columns. 

These  symptoms  are  due  to  alteration  of  the  white  substance  of  the 
cord,  and  have  been  termed  by  Charcot  "  symptomes  leucomyeliques." 
They  are  naturally  late  in  their  manifestation,  and  indicate  that  the  glioma 
has  passed,  in  its  influence,  beyond  the  bounds  of  the  gray  matter,  and  that 
it  or  the  resulting  cavity  intrenches  on  the  lateral  or  posterior  or  other 
columns  by  pressure  or  actual  degeneration. 

1.  Lateral  sclerosis  is  recognized  by  well-known  motor  symptoms. 
Symptoms  of  spastic  paralysis  may  be  of  all  grades  from  moderate  paresis 
with  some  stiffness  to  the  complete  stage  where  contracture  supervenes.  An 
early  indication  of  this  change  is  an  exaggerated  knee-jerk,  and  in  an 
advanced  case  the  addition  of  ankle-clonus.  In  sixty-one  cases  out  of  one 
hundred  and  eighteen  the  knee-jerk  was  plus. 

Spastic  symptoms  were  noted  in  our  list  of  one  hundred  and  eighteen 
cases  in  eighteen  instances. 


1  Transactions  of  tin-  A.merican  Psychological  Association,  December,  1894. 


44  GUY    HINSDALE,    M.D. 

2.  Symptoms  due  to  sclerosis  of  the  posterior  columns  or  tabetic  symp- 
toms are  thought  to  be  more  common  than  the  spastic  symptoms.  The 
well-known  distinguishing  signs  are  motor  incoordination,  defective  station 
with  eyes  open  or  closed,  lancinating  pains,  and  loss  of  knee-jerk.  We 
have  noted  tabetic  symptoms  in  nine  cases  out  of  one  hundred  and  eighteen. 
In  a  later  chapter  on  the  forms  of  syringomyelia  we  will  refer  to  this  sub- 
ject again.  In  one  hundred  and  eighteen  cases  the  knee-jerk  was  absent  in 
six,  diminished  in  four,  normal  in  twelve. 

Tactile  Sensibility. — This  is,  as  a  rule,  preserved  in  syringomyelia,  and 
constitutes,  by  its  presence  and  by  the  absence  of  pain  and  temperature 
sense,  the  well-known  "dissociation  symptom." 

In  some  analgesic  areas  there  is  occasionally  observed  a  lowering  of  the 
tactile  sense, — hyposesthesia.  This  is  tested  by  noting  whether  there  is  any 
deviation  or  disappearance  of  the  appreciation  of  ordinary  contact,  of  tactile 
pressure,  of  simultaneous  tactile  pressures,  of  the  appreciation  of  outline 
(relief),  and  of  the  tactile  perception  of  liquids. 

Absolute  tactile  ansesthesia  is  altogether  exceptional,  but,  of  course, 
where  complications  are  present  involving  the  white  matter  of  the  posterior 
columns,  we  naturally  would  expect  disturbances  of  tactile  sensation.  The 
allied  forms  of  sensation,  the  muscular  sense,  pressure  sense,  localization 
sense,  etc.,  are  almost  always  preserved  in  syringomyelia.  It  has  been 
claimed  that  in  some  cases  the  sensation  of  skin  pressure  was  entirely  absent 
or  at  least  very  much  diminished,  while  the  deeper  pressure  sensation  was 
normally  preserved. 

The  Paths  of  Sensory  Impressions. — This  subject  opens  a  very  interesting 
field  for  investigation,  and  one  where  many  discoveries  are  yet  to  be  made. 
Investigations  that  are  purely  anatomical  and  physiological  bearing  upon 
this  subject  have  received  considerable  aid  from  the  clinical  study  of  syrin- 
gomyelia. It  is  a  subject  that  also  interests  the  psychologist.  There  seems 
to  be  a  geueral  agreement  that  the  nerve  fibres  for  the  conduction  of  pain 
and  temperature  run  in  different  tracts  from  those  that  conduct  ordinary 
tactile  sensation.  Professor  SchifF  has  always  maintained  that  the  gray 
matter  conducted  thermal  and  painful  sensations,  while  the  posterior  col- 
umns conducted  the  tactile  and  muscular  sense.  Brown-Sequard  differen- 
tiates this  further,  declaring  that  the  central  part  of  the  gray  matter  serves 
for  the  conduction  of  the  sense  of  temperature,  its  posterior  and  lateral  parts 
for  that  of  pain,  while  the  posterior  columns  of  the  cord  convey  tactile  sen- 
sibility, all  three  forms  previously  decussating  in  the  median  line.  Gowers 
says  that  after  decussation  in  the  posterior  commissure,  the  fibres  subserving 
sensibility  to  pain  pass  upward  on  the  antero-lateral  ascending  tract,  and 
that  those  subserving  temperature  probably  pass  up  in  their  immediate 
vicinity.  Gowers  quotes  a  case  of  injury  to  the  cord  in  the  upper  cervical 
region  involving  the  lateral  column  and  gray  matter,  as  the  result  of  which 
there  was  an  entire  loss  of  sensibility  to  pain  on  the  side  of  the  body  oppo- 
site to  the  lesion  without  any  loss  of  tactile  sensibility.     "Experiments 


SYRINGOMYELIA.  45 

seem  to  show  that  tactile  sensibility  is  conducted  by  the  posterior  columns, 
and  the  integrity  of  these  latter,  especially  in  the  earlier  stages  of  the  dis- 
ease, would  account  for  its  retention  in  some  cases." 

ETIOLOGY. 

Sex. — Males  are  far  more  liable  to  syringomyelia  than  females.  Out 
of  one  hundred  and  ninety  cases,  one  hundred  and  thirty-three  were  in 
males  and  fifty-seven  in  females,  or  seventy  per  cent,  and  thirty  per  cent, 
respectively.  The  explanation  of  this  is  no  doubt  the  influence  of  trauma 
in  developing  an  innate  tendency  to  the  disease,  or  in  producing  directlv 
pathological  conditions  in  the  spinal  cord,  which  are  followed  by  glioma 
and  cavity  formation. 

Age. — The  influence  of  age  is  probably  active  in  great  measure,  as  per- 
mitting occupations  and  exposure  to  accident,  etc.,  which  act  directly.  The 
following  table  shows  the  frequency  in  the  different  decades  of  life  as  col- 
lected by  Schlesinger : 

Age.  Male.  Female.  Total. 

1  to  10 4  1  5 

11  to  20  36  8  44 

21  to  30  53  25  78 

31  to  40 30  12  42 

41  to  50 4  7  11 

51to60 3  3  6 

61+       3  1  4 

133  57  190 

The  decade  in  which  the  disease  is  most  frequently  observed  is  that  of 
twenty-one  to  thirty  years.  There  is  a  tendency  to  a  somewhat  later  de- 
velopment of  the  disease  in  women  than  in  men.  One  case  of  Schlesinger's 
(Obs.  xvi.)  occurred  in  a  woman  aged  seventy-eight  years. 

Occupation. — The  vast  majority  of  cases  occur  in  those  who  live  by 
manual  labor.     Overwork  is  frequently  noted. 

Trauma. — A  large  number  of  cases  are  apparently  the  result  of  injury, 
particularly  to  the  back.  We  may  mention  particularly  cases  of  Oppen- 
heira,  Strumpell,  Sinkler,  Stadelman,  Minor,  SokolofF,  Silcock,  Harcken, 
Bikeles,  Alexis  Thomson,  and  Eskridge. 

It  may  be  said  in  this  connection  that  Eickhorst  found  in  experiments 
on  animals  in  which  the  cord  had  been  divided  or  injured  that  cavities 
formed  frequently  in  the  posterior  columns,  and  sometimes  extended  into 
the  central  canal. 

In  cases  in  which  the  syndrome  in  syringomyelia  becomes  suddenly 
present,  especially  when  we  have  a  history  of  a  recent  trauma,  we  may 
naturally  suspect  the  existence  of  bsematomyelia,  since  hemorrhages  of  the 
spinal  cord  principally  affect  the  central  portion, — i.e.,  the  gray  Bubstance. 

The  production  of  glioma  in  consequence  of  trauma  requires  a  consid- 
erably longer  time.     It   is  quite  likely  that  traumatic  hemorrhages  of  the 


46 


GUY    HINSDALE,    M.D. 


Fig.  25. 


medulla  may  evolve  hemorrhagic  cysts,  which  would  then  have  compact 
surrounding  capsules  of  connective  tissue,  and  might  form  the  starting-point 
for  central  gliomatous  degeneration.  Such  a  pathogenic  process  may  also 
occur  when  the  central  hemorrhage  is  not  induced  by  trauma.  In  four 
cases,  in  which  the  organic  lesion  of  the  spinal  cord  undoubtedly  resulted 
from  trauma,  Minor  found  many  symptoms  closely  resembling  those  occur- 
ring in  syringomyelia :  for  instance,  the  characteristic  dissociation  of  sensi- 
bility. As  the  patients  in  question  are  still  living,  the  diagnosis  has  not 
been  confirmed.  In  a  fifth  case  of  traumatic  haeniatomyelia  death  occurred 
after  several  days.  The  autopsy  revealed  a  tubular  hemorrhage  throughout 
the  entire  gray  axis  of  the  spinal  column.1 

The  accompanying  figure  shows  the  arterial  circulation  for  the  cervical 
(0),  dorsal  (D),  and  lumbar  (L)  regions  of  the  cord. 

How  far  excess  in  alcohol  and  exposure  to  cold  and  dampness  are  fac- 
tors in  the  production  of  the  disease  we  cannot  say.     These  influences  are 

probably  of  small  moment.     It  has  been  noted 
by  Verhoogen  and  Vandervelden. 

Infectious  Diseases. — These  have  a  distinct 
predisposing  influence.  The  following  diseases 
have  been  observed  in  the  previous  history  of 
subjects  of  syringomyelia : 

Syphilis  (cases  of  Simon,  Schuele,  Neuhaus 
(Obs.  i.  and  v.),  Tornow) ;  rheumatism,  arthritis 
deformans  (Klemm) ;  typhoid  fever  (Bruhl,  Bern- 
hardt, Freund,  Westphal,  Schiippel,  Sokoloff, 
Schultze,  Remak) ;  tetanus  (Knoppek  and 
Meyer)  ;  variola  ;  erysipelas  of  the  head ;  chronic 
chorea  (Duchenne  and  Hoffmann) ;  Basedow's 
disease  (Joffroy  and  Achard) ;  pachymeningitis 
chronica  (Rosenblath,  Schmaus,  Francotte) ; 
myelitis  (Leyden) ;  anterior  poliomyelitis  (Kah- 
ler  and  Pick) ;  Friedreich's  disease  (Friedreich 
and  Dejerine,  Letulle). 

Heredity. — In  two  instances  syringomyelia 
seems  to  have  assumed  a  family  type.  Verhoogen 
and  Vandervelden  report  the  disease  occurring  in 
In  an  autopsy  on  one  of  these  cases  the  anterior 
and  posterior  horns  were  found  intact;  the  central  canal,  of  an  oval  form 
with  the  long  exis  transverse,  was  found  with  its  aperture  closed  and  the 
cavity  full  of  granular  exudate  and  cells  with  gray  nuclei  and  with 
cellular  debris.  In  the  mid-dorsal  region  there  was  sclerosis  of  the  ex- 
ternal part  of  the  lateral  column  and  of  the  columns  of  Burdach  and  Goll. 
The  canal  was  the  same  as  in  the  cervical  enlargement.     In  the  lumbar 


Arterial  circulation  in  the  spinal 
cord.    (Brissaud.) 


two  sisters  and  a  brother. 


Arcbiv  fur  Psychiatrie,  vol.  xxiv. 


SYRINGOMYELIA.  47 

region  there  was  sclerosis  of  the  postero-internal  part  of  the  anterior  column, 
and  in  the  whole  extent  of  the  lateral  column  and  the  anterior  portion  of 
the  column  of  Burdach  alteration  of  the  canal,  most  marked  in  the  upper 
portion. 

Dr.  Andrea  Ferrannini  has  recently  described  four  cases  in  one  family, 
including  two  brothers,  Nicola  and  Francesca,  their  sister  Martaand  mother 
Benedetta.  At  different  times  all  four  have  sought  medical  advice  for  the 
same  affection.  Panaris,  paresthesia,  and  special  forms  of  dysesthesia, 
limited  to  a  single  upper  extremity  or  abscess,  developed  without  any  ap- 
parent cause ;  felons  developed  in  the  left  thumb  of  the  two  brothers,  in 
the  right  thumb  in  the  mother,  and  in  the  right  index-finger  of  the  sister 
Marta.  In  Nicola,  Benedetta,  and  Marta  the  swelling  was  followed  by 
necrosis  and  complete  destruction  of  the  last  phalanx  in  each  case.  In  the 
fourth  patient  there  was  no  necrosis.  In  all  four  patients  the  incision  of 
the  swelling  by  the  physician  at  different  times  gave  exit  to  a  very  small 
quantity  of  pus  or  sometimes  only  to  blood.  Marta  felt  neither  the  incision 
nor  the  extraction  of  the  dead  bone,  much  to  the  wonderment  of  onlookers. 
These  manifestations  occurred  in  two  of  the  cases,  Nicola  and  Marta,  be- 
tween the  thirtieth  and  thirty-fifth  years,  and  in  the  others  at  about  the 
fiftieth  year. 

Panaritia  were  observed  in  all  four  patients,  and  the  ulceration  with 
acute  oedema  or  pseudophlegmon  of  the  forearm  were  noted  in  Nicola. 
There  were  marked  vasomotor  changes.  Appearance  of  erythromelalgia  in 
Francesca's  left  hand.  These  appearances  would  subside  at  times  and  the 
hand  would  suddenly  become  white  and  cold  as  though  dead,  then  painful 
at  times,  constituting  an  acrodynia  and  an  acroparesthesia,  hyperesthetic 
rather  than  anesthetic.  Disordered  sensation  to  temperature.  Heat  was 
recognized  as  cold  and  vice  versa.  Formication  in  the  calves  of  the  legs, 
ankles,  sole  of  the  foot  or  shoulder,  chiefly  on  the  left  side  of  the  body. 
Burning,  or  a  sense  of  cold,  in  the  first  three  fingers  of  the  left  hand  or  in 
only  one,  particularly  the  ungual  phalanx  of  the  thumb.  Frequently  at 
times  a  painful  sensation  as  from  many  pins  pricking,  or  stings  of  bees. 
Also  a  curious  sensation  in  the  ball  of  the  thumb.  These  sensations  pre- 
cede an  attack  of  erythromelalgia.  The  sensations  were  likened  to  the 
action  of  a  file  or  the  gnawing  of  an  animal ;  the  pain  was  deep  and  either 
intermittent  or  intensifying  towards  a  crisis.  The  pains  were  like  those  of 
syphilis  except  that  there  was  no  nocturnal  exacerbation  and  no  increased 
pain  on  pressure. 

A  little  ice  in  contact  with  the  thumb  gave  the  sensation  of  intense 
heat;  a  temperature  of  5°  C.  was  felt  as  hot;  at  other  points  of  the  body 
gave  the  sensation  of  contact  only.  On  the  other  hand,  there  was  complete 
loss  of  heat  sense,  even  when  tested  to  100°  C. 

Fibrillary  twitchings  present. 

Varieties. — The  great  diversity  of  forms  of  syringomyelia  renders  a 
classification  desirable.     We  may  have  types  as  follows: 

4 


48  GUY    HINSDALE,    M.D. 

1.  Atrophic  or  anteropoliomyelitic. 

2.  Spastic  and  amyotrophic  lateral  sclerosis. 

3.  Sensory  (posterior  and  median  poliomyelitic). 

4.  Type  M  or  van. 

5.  Lumbar  type. 

6.  Unilateral  type. 

7.  Bulbar  type. 

8.  Anterior  leucomyelitic  or  posterior  leucomyelitic. 

9.  Latent  form. 

10.  Non-typical  cases. 

Clinically,  we  may  say  that  there  is  a  gliomatous  form  beginning  early, 
— between  the  ages  of  fifteen  and  twenty-five.  At  quite  an  early  period 
cicatrices  from  painless  burns  are  found,  marking  the  early  appearance  of 
thermo-ansesthesia.  In  other  cases  amyotrophy  is  one  of  the  earlier  signs. 
The  early  stage  is  long,  but  steadily  progresses. 

In  the  myelitic  form  the  onset  is  later  in  life;  it  has  less  tendency  to 
progress,  and  may  remain  completely  stationary.  For  example,  in  a  case 
of  Charcot's,  the  early  symptoms,  appearing  at  the  age  of  forty  years,  as- 
sumed a  paraplegic  form,  with  cervical  location,  with  amyotrophy,  and 
with  sensory  and  trophic  disorders.  These  developed  rapidly  at  first,  and 
then  remained  stationary. 

Type  31orvan. — Morvau  and  Dejerine  still  claim  for  this  affection  a  dis- 
tinct identity,  but  most  authorities  classify  it  as  a  type  only  of  syringomye- 
lia. An  argument  for  its  identity  is  found  in  the  apparent  tendency  of  the 
disease  to  occur  frequently  in  certain  localities.  This  has  been  taken  to 
indicate  a  toxic  origin. 

Gombault's  case,  in  which  he  found  in  a  patient  with  Morvan's  disease 
a  peripheral  neuritis  with  slight  sclerosis  of  the  cervical  cord,  lends  some 
probability  to  this  theory ;  but  it  has  lately  been  shown  that  peripheral 
neuritis  may  occur  in  syringomyelia  as  well  as  Morvan's  disease,  and  that 
cavities  in  the  spinal  cord  may  occur  in  well-marked  cases  of  the  latter 
affection.1  (Joffroy  and  Achard.)  Thus  Morvan's  disease  is  held  to  be 
only  a  special  clinical  form  of  syringomyelia  characterized  by  predominance 
of  panaris. 

Unilateral  Gliomatosis. — It  is  not  unusual  for  the  gliomatosis  to  be  con- 
fined to  the  entire  gray  matter,  or  to  a  single  half  of  the  spinal  cord.  Such 
irregularities  naturally  give  rise  to  difficulty  of  diagnosis.  (See  Fig.  26.) 
(The  author  is  indebted  to  Dr.  Charles  K.  Mills  for  the  use  of  this  figure, 
taken  from  his  work  on  "  Nervous  Diseases,"  in  press.) 

(Cases  of  Oppenheim,  Rossolimo,  and  of  Dejerine  and  Sottas  and  Wein- 
traud  are  of  this  variety.) 

The  bulbar  type  has  already  been  considered. 

Tabetic  Type. — This  type  arises  from  a  combination  of  tabes  with  syrin- 

1  Soc.  Med.  des  Hopitaux,  1890  and  1891. 


SYRINGOMYELIA. 


49 


gomyelia,  or  by  an  extension  of  the  gliosis  to  the  posterior  columns.  Such 
cases  are  not  unusual,  and  have  been  recorded,  among  others,  by  Redlich, 
Eisenlohr,  Nonne,  Senator,  Mann,  Rosenblath,  Jegorow,  Schiippel,  Schle- 
singer  (Obs.  xii.). 

Fig.  26. 


Unilateral  glioinatois. 


In  a  recently  published  case  of  Oppenheim's  (Arehiv  fur  Psychiatrie, 
vol.  xxv.)  a  man,  aged  forty,  had  for  a  long  time  an  affection  characterized 
for  the  most  part  with  signs  of  tabes  (unsteadiness  of  gait,  and,  with  eyes 
closed,  increased  sway).  The  knee-jerk  was  absent  on  the  left  side.  There 
were  troubles  of  sensation,  with  dissociation  of  tactile  sensibility  and  ther- 
mic and  pain  sense,  and  scars  on  different  portions  of  the  skin.  The  sub- 
ject, who  had  kypho-scoliosis,  was  weak-minded,  and  had  ideas  of  grandeur, 
etc.  Dementia  paralytica.  Death  ensued,  and  at  the  autopsy  diffused 
glioma  of  the  spinal  cord  and  gray  degeneration  of  the  posterior  columns 
were  found.  Chronic  cerebral  pachy-  and  leptomeningitis  were  found,  dila- 
tation of  the  ventricles,  atrophy,  and  gray  degeneration  of  the  nerves  and 
optic  fibres  (bandelettes).  Central  gliomatosis  of  the  cord  and  posterior 
fascicular  degeneration. 

Glioma  of  the  lower  cervical  enlargement  extending  through  the  dorsal 
cord  to  the  lumbar  enlargement. 

In  the  mid-dorsal  region  the  entire  gray  substance  was  involved.  In 
the  lower  part  and  in  the  lumbar  region  the  gliomatous  product  was  con- 
fined to  the  left  half  of  the  cord. 

In  Oppenheim's  case  Clark's  column  was  atrophied  on  the  lef'f  by  com- 
pression and  atrophied  on  the  right  by  degeneration.     In  the  lower  part  of 


50  GUY    HINSDALE,    M.D. 

the  dorsal  cord  the  columns  of  Goll  were  degenerated.  Lower  down  the 
degeneration  is  diffused  throughout  the  two  posterior  fasciculi,  and  dimin- 
ished from  above  downward  to  the  lumbar  region.  The  degeneration  ot 
Clark's  column  occupied  in  the  same  extent  the  right  side,  while  the  left 
column  (the  side  of  the  lesion)  had  retained  its  normal  character. 

At  the  seat  of  the  lower  portion  of  the  glioma  the  degeneration  of  the 
posterior  right  column  was  still  active.1 

The  latent  form  of  syringomyelia  referred  to  by  some  authors  includes 
those  cases  where  no  manifestations  of  the  disease  were  noted  during  life, 
but  where  the  true  diagnosis  was  established  at  the  autopsy.  It  is  quite 
likely  that  if  these  unrecognized  cases  had  been  more  closely  studied  during 
life,  sensory  disorders  and  other  symptoms  would  have  been  given  their 
proper  weight.  It  would  seem,  therefore,  that  this  class  of  cases  would  be 
likely  to  play  a  less  conspicuous  part  in  the  classification  of  the  various 
forms  of  the  disease. 

It  has  been  claimed  that  in  the  latent  form  the  lesion  may  exist  in  the 
periependymal  region,  and  yet  there  be  no  disturbance  of  the  functions  of 
the  white  or  gray  matter  of  the  cord.  A  lesion  localized  on  one  side  may 
not  necessarily  be  revealed  in  any  objective  symptoms  referable  to  that 
locality,  for,  although  we  are  not  able  to  say  just  how  far  compensation  may 
exist  or  what  the  channels  of  commissural  innervation  may  be,  it  is  reason- 
able to  believe  that  the  function  of  one  side  may  be  more  or  less  completely 
performed  by  corresponding  nerve-cells  of  the  opposite  side  by  means  of 
commissural  communications,  which  physiologists  teach  us  have  an  exist- 
ence. We  are  not  in  a  position  as  yet  to  state  just  how  these  commis- 
sures act. 

SYRINGOMYELIA  ASSOCIATED   WITH   OTHER   DISEASES. 

Hysteria. — A  few  of  the  reported  cases  present  hysterical  symptoms. 
An  excellent  example  is  that  reported  recently  by  Dr.  Agostiui,  of  Perugia. 
The  woman  was  thirty-five  years  old,  and  gave  a  family  history  of  alco- 
holism, phthisis,  and  nervous  derangements.  Her  present  illness  began 
four  years  ago  with  neuralgic  pains  in  the  left  scapular  region,  and  with 
formication  and  a  feeling  of  weight  and  debility  in  the  arms,  first  affecting 
the  pectoral  region,  then  the  arms,  forearms,  and,  lastly,  the  hands.  At  the 
same  time  she  developed  hysteria,  paraplegia,  and  aphasia,  and  later  on  the 
classical  convulsions  of  hysteria  major.  These  symptoms  persisted  for  two 
years,  and  were  finally  treated  successfully  by  hypnotism. 

Muscular  force  of  right  hand,  thirty ;  of  left,  five.  Marked  atrophy 
of  the  muscles  of  the  forearm,  of  the  interossei,  and  of  the  thenar  and  hypo- 
theuar  eminences. 

Tactile  sensibility  is  generally  preserved,  sasTe  on  the  posterior  part  of 


Archiv  fiir  Psychiatrie,  1893,  vol.  xxv.  p.  315. 


SYRINGOMYELIA.  51 

the  left  upper  arm,  where  hyperesthesia  is  present.  Sensation  of  heat  and 
cold  and  of  pain  are  abolished  from  the  neck  to  the  ninth  intercostal  space 
and  in  the  left  arm.  Muscular  sense  is  intact,  likewise  sense  of  taste,  sight, 
and  hearing.  Visual  fields  concentrically  contracted.  Pupils  do  not  react. 
Exaggeration  of  the  muscle  and  tendon  reflexes.  Reaction  of  degenera- 
tion in  the  muscles  of  the  thenar  and  hypothenar  eminences. 
Agostini  concludes  as  follows  : 

1.  Syringomyelia  may  be  associated  with  hysteria,  and  confusion  may 
arise  when  the  difference  pertains  to  sensibility  alone. 

2.  The  presence  of  progressive  muscular  atrophy,  accompanied  by  di- 
minished electrical  excitability,  persistence  of  the  muscular  sense,  point  to 
a  syringomyelic  affection  rather  than  an  hysterical. 

3.  The  best  diagnostic  criterion  in  this  and  other  neuropathic  affections 
is  hypnosis,  in  which  muscles  with  anatomical  lesions  do  not  pass  into  the 
cataleptic  state. 

Cases  of  syringomyelia  and  hysteria  have  been  recorded  by  Charcot  and 
Asmus. 

Syphilis  of  the  Central  Nervous  System. — This  has  been  observed  in  con- 
nection with  syringomyelia  by  Eisenlohr,  Nonne,  Jegorow,  Beevor,  Sou- 
ques  (339),  Sinkler  (333),  Rosen blath  (303). 

It  is  liable  to  give  rise  to  difficulties  in  diagnosis. 

Lepra. — A  vigorous  controversy  has  arisen  as  to  the  relation  of  this 
disease  to  cases  reported  as  syringomyelia,  particularly  of  the  type  Morvan. 
Zambaco  and  others  have  maintained  that  Morvan's  disease,  so  called,  is 
nothing  more  than  anesthetic  leprosy.  There  is  no  doubt  that  a  strong 
analogy  does  exist  in  some  cases  between  the  symptoms  of  these  affections 
and,  to  a  less  extent,  scleroderma,  ainhum,  the  tropho-neuroses,  morphoea, 
and  symmetrical  gangrene.  In  discussing  this  subject  before  the  Sociedade 
das  Sciencias  Medicas  of  Lisbon,  Dr.  Falcao  expressed  the  opinion  that 
Morvan's  disease  and  syringomyelia  are  in  reality  anesthetic  leprosy,  but 
he  believes  that  the  other  affections  cannot  be  classed  with  this  disease. 
Dr.  Falcao  was  consulted  by  a  patient  from  Para  who  presented  the  fol- 
lowing symptoms :  Atrophy  of  the  thenar  and  hypothenar  eminences,  in- 
terossei,  and  some  muscles  of  the  forearm,  anesthesia,  bent  fingers,  and 
thickening  of  the  ulnar  nerve.  Dr.  Falcao  made  the  diagnosis  of  lepra 
anesthetica,  which  was  justified  not  only  by  the  symptoms  present,  but  by 
the  fact  that  the  patient  came  from  a  country  where  leprosy  is  a  common 
disease.  Subsequently  this  patient  went  to  Paris  to  consult  Professor 
Charcot,  from  whom,  it  is  said,  he  received  a  written  statement  to  the  effect 
that  the  disease  in  question  was  syringomyelia. 

The  Gazcta  Medica  da  Bahia  relates  the  celebrated  case  of  a  French- 
man named  Mares,  who  for  more  than  seven  years  appeared  in  the  hospitals 
of  Paris  as  a  case  of  Morvan's  disease.  Professor  Hayem  and  Monod  con- 
firmed this  diagnosis,  and  the  latter  amputated  several  fingers  of  Mares,  and 
published  in  the  Archives  de  Midecine  et  de  Chirurgie  his  observation-  i 


52  GUY    HINSDALE,    M.D. 

this  case,  which  he  regarded  as  a  typical  one  of  Morvan's  disease.  Later 
on,  Broca  confirmed  the  previous  diagnosis  and  amputated  two  fingers  of 
this  patient.  Again  Hay  em  took  charge  of  him,  and  amputated  another 
finger.  Several  months  later  Mares  was  admitted  to  the  Saltpetriere,  where 
Professor  Charcot  had  him  photographed,  and  for  eleven  months  exhibited 
him  to  physicians  and  students  as  a  case  of  Morvan's  disease.  Later  on, 
Charcot  diagnosed  Mares's  case  as  syringomyelia,  type  Morvan.  Finally, 
this  patient  was  admitted  to  the  Hospital  de  Bicetre,  where  Dejerine  did 
not  agree  with  Charcot  as  to  the  identity  of  these  two  affections,  and  stated 
that  Mares  had  simply  Morvan's  disease.  Gombault,  who  had  made  several 
histological  examinations  of  the  amputated  fingers  of  Mares,  admitted  the 
diagnosis  of  Dejerine, — Morvan's  disease.  Dr.  Zambaco  procured  the  address 
of  Mares,  and,  after  examining  him  at  his  residence,  he  was  convinced  that 
he  had  before  him  a  case  of  leprosy.  In  this  it  is  reported  that  he  was 
sustained  by  Vidal,  Besnier,  Tournier,  Hallopeau,  Quinquaud,  Du  Castel, 
aud  Tenneson.1 

A  genuine  case  of  syringomyelia  associated  with  leprosy,  confirmed  by 
both  a  bacteriological  examination  and  an  autopsy,  has  been  recorded  by 
Souza-Martin  and  L.  da  Camara  Pestana.  (See  case,  Semaine  Medicate, 
No.  20,  1894.)  The  autopsy  revealed  in  the  cervical  region  a  cavity  in- 
volving the  gray  and  white  substance.  The  cavity  was  filled  with  a  brown, 
diffluent  mass.  In  preparations  of  this  substance  stained  by  immersion  for 
six  minutes  in  the  carbolized  fuchsine  of  Ziehl,  then  decolorized  by  nitric 
acid,  he  was  able  to  find  a  great  number  of  bacilli  disposed  iu  groups  of 
the  length  of  four  /*,  presenting  clear  spaces  separated  by  strongly  colored 
granulations  which  were  found  usually  at  the  extremity  of  the  bacillus. 
These  characters  are  those  of  the  bacillus  of  Hansen  (lepra). 

In  this  instance  a  case  of  syringomyelia  diagnosticated  two  years  before 
death  has  confirmed,  for  the  first  time,  the  ideas  enunciated  by  Zambaco. 

While  it  is  not  possible  to  conclude  from  this  one  case  the  etiologic  unity 
of  syringomyelia  and  leprosy,  it  leads  us  to  recognize  that  the  syringomyelic 
affection  of  the  type  Morvan  may  afford  an  easy  entrance  for  the  bacillus 
of  lepra. 

In  leprosy  with  nervous  disturbance  the  disease  seems  to  depend  on  a 
neuritis, — i.e.,  that  tactile  sensibility  is  involved  as  well  as  the  other  forms 
of  sensibility.  In  very  rare  cases, — e.g.,  that  of  Rosenbach, — we  find  at 
the  seat  of  the  macules  preservation  of  tactile  sense  with  alteration  of 
temperature  and  pain  sense. 

The  distinguishing  features  are  as  follows  : 

Syringomyelia. — Disassociation  of  sensory  disturbances;  integrity  of 
superficial  muscles  of  the  face;  absence  of  discolorations  on  the 
skin  ;  hair  unaffected  ;  deviations  of  the  spine. 

1  See  article  by  Dr.  Alvarez,  of  Hawaii,  Pacific  Medical  Journal,  January,  1895. 
Also  Semaine  Mtklicale,  1893,  pp.  289,  295. 


SYRINGOMYELIA.  53 

Anoesthetic  Leprosy. — Abolition  of  tactile  sense;  atrophy  and  paresis 
of  the  superficial  muscles  of  the  face;  thickening  and  nodulous 
swellings  of  nerves;  discolorations  (painless)  upon  the  body. 
Zones  of  anaesthesia  and  thermo-anaesthesia  irregularly  distributed 
in  the  shape  of  plaques  with  sharp  transition  from  the  affected 
to  the  normal  areas. 

These  spots  or  islets  of  anesthesia  are  circumscribed  by  a  reddish  line  a 
little  raised  and  very  irregular. 

In  syringomyelia,  on  the  contrary,  the  anesthetic  zones  of  thermo- 
anesthesia occupy  large  areas  limited  by  regular  lines. 

Souza-Martin  goes  to  the  extreme  in  denying  that  syringomyelia  is  a 
nosological  entity,  and  affirms  that  it  is  merely  a  condition  that  confronts  us 
and  not  a  disease  per  se.  He  attempts  to  claim  that  it  is  similar  in  a  certain 
sense  to  cavernous  affections  in  the  lungs,  which  he  says  we  might  just  as 
well  call  syringopneumia ;  in  other  words,  the  condition  known  as  syringo- 
myelia may  be  present  in  various  diseases,  among  which  he  reckons  leprosy. 
It  is  needless  to  say  that  we  dissent  entirely  from  his  views. 

As  to  the  relationship  of  lepra  and  syringomyelia  we  believe  that  an 
individual  who  may  exhibit  symptoms  of  syringomyelia  or  Morvan's  disease 
may  have,  in  addition,  leprosy.  For  example,  this  was  recently  observed 
by  Pitres  and  Sabrazes  in  what  they  report  as  a  case  of  systematic  nervous 
leprosy  of  syringomyelic  type.  It  required  a  bacteriological  examination 
to  determine  its  real  nature.  To  accomplish  this  it  was  necessary  in  one 
case  to  excise  a  portion  of  the  neuritic  nerve  from  the  living  subject.  The 
bacillus  was  found  in  large  numbers,  limited,  however,  to  the  nerve-fasciculus 
itself,  none  being  found  in  the  perineurium,  the  intrafascicular  tissue,  or  in 
the  vessels. 

In  three  other  cases  where  the  bacillus  was  searched  for  and  not  found 
the  conclusion  was  reached  that  leprosy  and  syringomyelia  are  distinct  effec- 
tions,  both  as  to  etiology  and  nature,  notwithstanding  that  certain  analogies 
are  present  in  their  symptoms.  The  weight  of  authority  is  in  favor  of  the 
duality  of  the  diseases,  Zambaco  being  the  principal  claimant  for  their 
identity. 

Syringomyelia  and  Chronic  Hydrocephalus. — This  combination  points  to 
the  developmental  origin  of  syringomyelia.  Out  of  one  hundred  and 
thirty  reported  cases  examined  Rupfer berg  found  fifteen  in  which  a  syringo- 
myelia or  hydroinyelia  accompanied  a  chronic  idiopathic  hydrocephalus. 
The  cases  of  syringomyelia  were  those  of  Langhans  (4),  Westphal, 
Kiewlicz  (1),  Chiari  (2),  to  which  we  add  those  of  Voughl  and  Schlesinger 
(Obs.  13).  The  latter  has  also  recorded  a  case  of  hydrocephalus,  idiocy, 
and  syringomyelia  combined.     (Obs.  29.) 

Spina  Bifida. — This  affection  furnished  the  cases  in  which  some  of  the 
earliest  observations  of  syringomyelia  were  made.  It  is  more  distinctly 
related,  however,  to  hydroinyelia.     (See  cases  of  Pagenstecher.) 


54  GUY    HINSDALE,    M.D. 

Tumors  of  the  pons,  cerebellum,  and  cerebrum  have  been  found  in  cases 
reported  by  Gowers,  Harris,  Kronthal,  Hoffmann,  and  Schultze. 

Cervical  Hypertrophic  Pachymeningitis. — In  Rosenblath's  case  this 
was  believed  to  be  the  primary  condition  and  the  syringomyelia  to  have 
developed  later.  Other  cases  have  been  reported  by  Raymond  and  Critz- 
man. 

Acromegaly  and  Cheiromegaly. — Marie  exhibited  about  a  year  ago 
before  the  Medical  Society  of  the  Hospitals  of  Paris  a  case  of  this  character. 
The  patient  was  a  young  man  of  twenty-one,  having  syringomyelia.  His 
right  hand  and  left  foot  had  for  some  years  been  much  increased  in  size. 
Charcot  and  Brissaud  have  also  described  a  form  of  trophic  affection  of  the 
bone  under  the  name  of  cheiromegaly,  which,  as  the  name  implies,  is  an 
increase  in  the  size  of  the  hands  and  fingers  analogous  to  acromegaly. 
Holschevnikoff  and  Recklinghausen  have  described  cases  of  syringomyelia 
with  acromegaly;  it  is  quite  likely  that  the  latter  is  only  a  trophic  disturb- 
ance entirely  secondary  or  a  part  of  the  primary  syringomyelia.  Hoffmann 
(Obs.  12)  and  Karg  have  published  similar  cases.  (See  Frederick  Peter- 
son's case.) 

Amyotrophic  Lateral  Sclerosis. — Lloyd's  case.  (See  Figs.  8,  9,  10, 
and  13.) 

Friedreich's  Ataxia. — This  disease  is  probably  closely  related  to  syringo- 
myelia. The  motor  symptoms,  the  spinal  curvature,  the  trophic  and  vaso- 
motor symptoms,  to  a  slight  extent  the  sensory  disorders,  the  bulbar  symp- 
toms, and  particularly  the  nystagmus,  all  point  to  the  intimate  relationship 
of  the  two  affections.  Further  than  this,  in  three  out  of  the  twelve 
autopsies  in  cases  of  Friedreich's  ataxia  collected  by  Griffith  cavities  have 
been  found. 

Among  other  diseases  which  have  been  noted  in  connection  with  syrin- 
gomyelia we  have  Basedow's  disease  (Joffroy  and  Achard),  pellagra  (Pel- 
lizi),  Friedreich's  disease  (Friedreich,  Dejerine,  Letulle),  general  paralysis 
and  dementia  (Fiirstner  and  Zacher,  Kanasugi,  Hoffmann,  Czerny),  chronic 
chorea  (Duchenne  and  Hoffmann),  idiocy  (Arndt),  melancholia  (Schuele, 
Meyer),  mania  (Defoix),  and  cancer  of  the  stomach  (Jeffries). 

The  mental  state  is,  as  a  rule,  undisturbed  unless  bulbar  involvement 
ensues. 

DIAGNOSIS. 

So  much  has  been  said  in  the  foregoing  chapter  on  the  relation  of  this 
to  other  diseases  that  a  full  discussion  would  involve  much  useless  repeti- 
tion. It  may  be  said  in  general  that  the  diagnosis  of  syringomyelia  now 
rests  upon  a  firm  foundation,  and,  in  a  classical  case,  ought  to  present  no 
difficulty  in  forming  a  correct  opinion  during  life.  In  fact,  the  diagnosis  is 
repeatedly  made  intra  vitam  and  corroborated  at  the  autopsy,  and  that  too 
in  cases  that  depart  in  some  degree  from  the  typical  form.  It  naturally 
happens  that  where  trophic  changes  assume  prominence,  or  in  cases  of  amy- 


SYRINGOMYELIA. 


00 


otrophy  or  amyotrophic  lateral  sclerosis,  or  those  cases  in  which  the  disease 
is  said  to  be  latent,  difficulties  will  arise.  But,  whatever  the  predomi- 
nating form,  we  must  depend  for  our  diagnosis  and  lay  great  stress  on  the 
more  characteristic  signs  of  the  disease,  particularly  sensory  troubles  and 
the  dissociation  symptom.     This  is  not,  however,  an  infallible  guide. 

Fig.  27. 


Syringomyelia.— Showing  analgesia  (vertical  lines),  thermoanesthesia  (oblique  lines),  tactile  anses* 
thesia  (horizontal  lines).    This  case  was  associated  with  amyotrophic  lateral  sclerosis. 

Clinical  observations  prove  that  the  dissociation  of  sensibility  exists  in 
circumscribed  neuritis  or  polyneuritis  as  well  as  in  the  neuritis  of  leprosy 
(Leloir,  Babinski,  Thibierge,  Pitres  and  Sabrazes,  ChafTard,  Rosenbach, 
Ziehl,  Nothnagel,  Ferrannini),  in  alcoholic  neuritis  (Lancereaux,  Lemoine), 
in  neuritis  with  tabetic  symptoms  (Joffroy  and  Du  Cazal  and  Parmentier), 
and  in  the  neuritis  following  trauma,  as  in  a  case  of  Charcot's. 

In  this  instance  a  gunshot  wound  of  the  neck  produced  an  injury  to  the 
nerve-roots  with  the  occurrence  of  thermo-ainesthesia.1  Lloyd's  cases  of 
traumatic  affections  of  the  spinal  cord  are  also  cases  in  point. 

As  a  rule,  the  dissociation  symptom  is  observed  in  all  reported  cases, 
but  there  are  a  few  in  which  this  symptom  is  not  stated  to  have  been  ob- 
served, but  where  other  important  disorders  of  the  nervous  system  have 
existed,  and  at  the  autopsy  a  syringomyelia  was  found  (Schuele,  Striimpell, 
Schultze,  Schlesinger,  Obs.  6).  Unless  one  makes  a  practice  of  exam- 
ining in  a  careful  manner  the  state  of  the  various  kinds  of  sensibility  in  all 
cases  of  nervous  disease,  it  will  be  quite  likely  that  cases  of  syringomyelia 
will  be  allowed  to  pass  as  hypochondriac,  neurasthenic,  or  as  suffering  from 


1  Clinique  des  Maladies  du  Systeme'nerveux,  Paris,  1892,  p, 


56  GUY    HINSDALE,    M.D. 

neuritis,  arthritis,  etc.  Cases  of  unusual  joint-disease  should  always  excite 
our  suspicions,  and  should  be  tested  for  therrno-anaBsthesia  and  analgesia. 
So  also  in  any  case  of  spontaneous  fracture  or  repeated  dislocation  in  a  case 
of  arthropathy. 

On  the  other  hand,  a  diagnosis  of  syringomyelia  may  be  erroneously 
made  in  instances  of  syphilitic  tumors  of  the  spinal  cord.  Such  a  case  has 
been  recorded  by  Dr.  Beevor,  of  London.  A  gardener,  aged  fifty  years, 
after  two  days'  exposure  to  wet  in  July,  1892,  began  to  drag  the  left  leg. 
In  a  few  hours  he  had  weakness  of  the  left  arm  and  numbness  of  the  right 
knee.  "He  noticed  the  weakness  of  the  left  limbs  for  a  fortnight  before 
admission,  as  well  as  wasting  of  the  left  arm."  On  the  right  side  the  numb- 
ness spread  up  to  the  groin,  and  during  the  last  fortnight  to  the  nipple. 
He  had  no  pain  till  a  week  after  the  onset  of  the  symptoms,  when  he  began 
to  have  pain  in  the  left  shoulder,  elbow,  and  wrist,  and  numbness  in  the 
left  thumb  and  radial  border  of  the  forearm.  There  was  no  affection  of  the 
sphincters,  and  no  history  of  gonorrhoea  or  syphilis.  On  admission  into 
the  National  Hospital  for  the  Paralyzed  and  Epileptic,  in  September,  1892, 
he  had  wasting  of  both  the  upper  limbs,  especially  the  left,  with  marked 
wasting  and  loss  of  power  in  the  left  serratus  magnus,  supinator  longus, 
muscles  of  the  forearm,  and  intrinsic  muscles  of  the  left  hand,  as  well  as 
weakness  of  the  left  lower  limb,  so  that  he  could  only  just  raise  the  leg  off 
the  bed.  Sensation  was  lost  to  pain,  heat,  and  cold  of  the  whole  of  the 
right  leg  and  the  right  half  of  the  trunk  up  to  the  fourth  rib,  while  tactile 
perception  was  normal.  The  knee-jerk  was  excessive  on  the  left  side,  and 
left  ankle-clonus  was  present.  Later,  the  loss  of  painful  sensation  spread 
up  to  the  right  arm  (ulnar  border)  and  left  forearm,  involving  the  radial 
border.  There  was  loss  of  electrical  reactions  in  the  intrinsic  muscles  of 
the  hand.  Later,  he  had  paralysis  of  the  sixth  nerve  of  the  right  side,  and 
he  gradually  became  worse,  and  died  on  November  14.  On  examination 
post  mortem,  two  syphilitic  tumors  were  found  on  either  side  of  the  brachial 
enlargement  of  the  cord,  the  left  one  passing  nearer  the  cord  than  the  right, 
but  the  cord  was  too  soft  for  accurate  examination. 

The  following  statement  of  the  similarity  of  symptoms  and  of  points  of 
divergence  will  be  useful  in  distinguishing  syringomyelia  from  atrophic 
paralyses : 

Progressive  Mus-  Amyotrophic 

cular  Atrophy.  Lateral  Sclerosis.     Syringomyelia. 

Age 25  to  35.  25  to  35.  20  to  45. 

Sex Male.  Male.  Male. 

Onset Gradual.  Gradual.  Gradual. 

Course Progressive.  Progressive.      Progressive  with 

remission. 
Muscular  atrophy Marked.  Marked.  Marked    in    the 

arms. 

Tactile  sense Intact.  Intact.  Intact. 

Pain  sense Normal.  Normal.  Lost. 

Temperature  sense Normal.  Normal.  Lost. 

Tendon  reflexes Diminished  or  0. 


SYRINGOMYELIA.  57 

COURSE  AND  PROGNOSIS. 

The  disease  is  essentially  a  chronic,  afebrile  one,  lasting  generally  for  a 
considerable  length  of  time.  Patients  have  been  known  to  live  forty  years 
after  the  onset  of  the  symptoms.  Remissions  are  liable  to  occur  in  the 
course  of  the  disease,  and  at  least  two  patients,  one  of  Bruhl  and  one  of 
Schlesinger,  have  died  at  the  age  of  seventy-three  years.  Harcken,  how- 
ever, believed  that  he  saw  it  take  an  acute  course  in  one  instance.  The 
prognosis  is  unfavorable.  Death  may  come  gradually  by  progress  of  the 
disease,  producing  cachexia,  emaciation,  bed-sores,  etc.,  or,  particularly,  by 
the  aggravation  of  certain  symptoms  of  the  disease,  such  as  trophic  dis- 
turbances, panaris,  phlegmon,  or  vesical  disorders.  Intercurrent  affections, 
such  as  tuberculosis,  etc.,  are  common  terminations. 

TREATMENT. 

Medical. — Pain  very  commonly  demands  relief.  Owing  to  the  chronic 
nature  of  the  malady  it  is  better  to  rely  on  preparations  like  antipyrin, 
acetanilid,  or  phenacetin  than  to  begin  the  use  of  opium.  Bromides  and 
chloral  will  also  be  occasionally  required.  Lukewarm  baths  are  often  of 
considerable  use.  Revulsive  applications  of  hot  and  cold  water  along  the 
spine  are  sometimes  useful,  but  care  has  to  be  taken  on  account  of  the  lia- 
bility to  trophic  disorders  of  the  skin.  On  this  account  the  cautery  would 
be  liable  to  give  trouble.  Tonics,  such  as  iron  and  arsenic,  phosphide  of 
zinc,  nitrate  of  silver,  and  iodide  of  potassium,  have  all  been  used  to  palliate 
the  condition. 

Surgical. — Local  treatment  for  panaris  or  ulcers  on  the  extremities,  for 
cracks  or  slowly-healing  sores  the  result  of  unfelt  burns,  and  for  boils  will 
be  demanded.  It  is  for  the  relief  of  these  affections  that  patients  commonly 
consult  a  physician  or  surgeon.  It  is  important  to  secure  the  healing  of 
obstinate  cracks  and  fissures  so  as  to  prevent  septic  infection.  The  analgesic 
skin  should  be  protected  from  injury.  It  will  be  necessary  to  avoid  hard 
labor,  and,  to  counteract  atrophy,  it  will  be  useful  to  use  massage  and  electri- 
cal stimulation. 

In  cases  where  arthropathy  with  fluid  develops,  a  surgeon  may  be  needed 
either  to  aspirate  the  affected  joint  or  for  the  removal  of  inconvenient  osteo- 
phytes or  for  the  closing  of  a  persistent  sinus.  In  an  extreme  case  resection 
of  the  joint  has  been  required.  Surgical  operations,  however,  arc  attended 
with  more  risk  in  these  cases  than  in  ordinary  subjects. 

CASES. 

CASE  I. — Robert  C,  colored,  aged  thirty-one,  bom  in  the  United  Slates  ;  weight 
one  hundred  and  eighty  pounds,  height  medium;  previous  occupation,  boot-black. 

Father  drowned  ;  mother,  alive;  three  sisters  died  <»('  phthisis. 

He'gives  a  history  of"  erysipelas"  in  infancy  ;  otherwise  the  patient  has  always 
been  healthy,  but  has  been  an  extensive  masturbator.  He  denied  syphilis  or  gonor- 
rhoea. At  the  age  of  ten  he  was  run  over  by  a  heavy  wagon,  his  right  leg  being 
severely  injured. 


58 


GUY    HINSDALE,    M.D. 


Fig.  28. 


The  present  disease  began  when  sixteen  years  of  age.  He  says  that  his  right 
shoulder  began  to  fall  and  that  this  was  accompanied  by  a  feeling  of  excessive  weak- 
ness in  the  left  side.  About  six  months 
after  this  he  began  to  limp  in  walking  as 
though  he  had  stubbed  his  toe.  A  year 
later  he  noticed  a  feeling  of  weight  in  his 
left  side.  This  gradually  grew  worse  so 
that  when  blackening  boots  he  had  great 
difficulty  in  polishing  the  left  side,  and  his 
brush  would  continually  fall  from  his  left 
hand.  This  continued  for  about  five  years. 
During  this  time  he  was  compelled  to  use  a 
cane.  His  right  hand  did  not  seem  to  be 
affected  at  this  time.  About  four  years  ago 
he  noticed  a  tendency  to  flexion  of  the 
fingers  of  the  left  hand, — a  claw-like  con- 
tracture,— main-en  -griffe. 

Two  years  later  the  right  hand  became 
similarly  effected.  He  has  never  had  any 
pain  in  his  lower  limbs. 

Sensory  disturbances  began  three  years 
ago. 

S.  P. — The  patient  is  a  well-nourished, 
rather  intelligent,  light-colored  negro.  As 
seen  in  the  accompanying  photograph,  taken 
at  the  Philadelphia  Hospital,  and  furnished 
together  with  the  following  notes  through 
the  kindness  of  Dr.  Dercum,  he  sits  in  a 
rolling  chair  during  the  day,  since  he  is 
unable  to  walk  or  to  move  his  arms.  He 
has  very  limited  motion  of  the  fingers,  particularly  those  of  the  left  hand.  The 
fingers  of  both  hands  are  strongly  contracted,  as  seen  in  the  photograph,  presenting 
the  typical  contracture  of  main- en- griffe.  There  is  atrophy  of  both  upper  extremities, 
but  more  on  the  left  side.  The  extensors  of  the  forearm  are  wasted  more  than  the 
flexors.  The  thenar  and  hypothenar  eminences  and  the  interossei  muscles  are  mark- 
edly atrophied.  The  man  is  quite  helpless  and  is  unable  to  move  from  side  to  side 
when  placed  on  his  back.  There  is  an  aggravated  scoliosis  with  convexity  to  the 
left.  The  tongue  is  protruded  straight,  but  shows  a  slight  atrophy  to  the  right  side 
with  fibrillary  twitching.  He  is  unable  to  swallow  perfectly,  and  has  more  difficulty 
with  solid  food. 


Reflexes.  Right. 

Plantar Present. 

Ankle-clonus  -f 

Knee-jerk -j- 

Cremasteric  Present. 

Muscle-jerk  -f- 

Epigastric   0 

Abdominal 0 

Contralateral  reflex  of  adductors....  Present. 


Left. 

0 
0 
Slight. 


Eye  examination,  January  23,  1895.     Pupils  normal ;  no  paralysis  of  external 
ocular  muscles;  fundus  normal;  optic  disks  normal. 

The  sensory  changes  are  well  seen  in  the  accompanying  charts. 


SYRINGOMYELIA. 


59 


There  is  partial  analgesia  over  the  entire  surface  of  the  body,  excepting  in  the 
posterior  aspect  of  the  left  forearm,  and  in  a  smaller  area  in  the  right  lumbar 
region,  limited  by  the  lumbar  spine,  the  tenth  rib,  and  the  right  iliac  crest.  In  these 
regions  the  pain  sense  is  normal.  Analgesia  is  complete  in  the  right  hand  and  wrist, 
posterior  aspect  of  the  left  hand  and  left  arm  and  right  leg,  and  in  the  anterior  aspect 
of  the  left  lower  extremity.     (See  Fig.  29.) 

Fig.  29. 


Sensory  changes  in  Case  I.,  Robert  Collins.— Tliermo-ancesthesia,  oblique  lines ;  confusion  of  sensation, 

circles ;  analgesia,  vertical  lines. 


There  is  total  thermo-amesthesia  in  the  right  arm  and  hand  [and  right  side  of 
the  posterior  thorax,  in  the  left  neck  and  shoulder  posteriorly,  and  over  the  right 
anterior  side  of  the  waist  nearly  to  the  middle  line.  It  will  be  noticed  that  this 
area  is  not  quite  superimposed  upon  an  area  of  analgesia  at  about  the  same  situa- 
tion. Over  the  anterior  surface  of  the  left  forearm  there  is  confusion  of  the  thermic 
sense  (represented  by  small  circles  in  the  figures),  heat  being  designated  cold,  and 
cold,  heat. 

Case  II. — Joseph  Shiselbaer,  aged  fifty-two,  German  tailor. 

Father  died  at  sixty-five  years  of  a  paralytic  stroke.  Mother  died  of  senility  at 
sixty-seven.  Drinks  a  little;  syphilis  denied.  In  the  summer  of  1890  lost  his  appe- 
tite, became  costive,  and  felt  unwell.  In  December,  1891,  he  gradually  lost  feeling  in 
the  right  hand  and  arm  and  could  not  do  his  work.  He  never  lost  power.  Later  he 
losl  power  of  feeling  in  the  left  hand.  Sensation  of  pins  and  needles  in  both  hands 
and  arms,  also  in  the  legs.  Arms  and  legs  also  cold.  He  never  had  severe  pain. 
Since  December,  1891,  was  lmrned  many  times  on  the  hands  and  arms  without  feeling 
it.     Is  very  emotional. 

S.  P. — A  well-built  man.  No  atrophy.  Pain  on  pressure  in  both  axillae.  No 
pain  over  the  median  or  ulnar  nerves.  Spine  straight;  no  pain  on  flexion  of  spine  or 
on  pressure.  Scars  from  burns  on  index  finger  and  thumb  of  the  right  hand.  The 
right  metacarpophalangeal  joint  of  the  thumb  is  enlarged  and  not  painful. 

Reflexes. — Elbow-jerk  gone  on  both  sides.     Knee-jerk.     No  true  clonus. 


60  GUY    HIKSDALE,    M.D. 

Eyes. — Pupils  equal  ;  small,  react  to  light  and  accommodation.  No  change  in 
form  fields. 

Dynamometer:  Right  76  ;  left  100. 

No  palsy  in  arms.  Some  trouble  in  touching  the  fingers  and  nose.  Fibrillary 
twitchings  of  muscles  of  right  forearm.  Heat  and  cold  sense  on  the  right  side  not 
distinguished  on  the  tips  of  the  fingers,  but  he  can  distinguish  at  base  of  fingers  on 
the  palmar  aspect. 

The  patient  distinguished  heat  and  cold  well  on  the  anterior  surface  of  the  arm, 
not  so  well  on  the  posterior  surface.  Left  hand  same  as  right.  At  the  base  of  the 
fingers  feels  heat  only.  In  the  anterior  aspect  of  the  fingers  can  recognize  both  heat 
and  cold.  Thermo-anaesthesia.  In  little  finger  (dorsal  surface  of  left  side)  hot  is 
called  cold.     Cold  always  felt  and  judged  correctly,  even  in  anaesthetic  areas. 

Confusion  of  sensation  of  heat  and  cold  on  palmar  surfaces  of  both  hands.  Hot 
invariably  called  cold  on  the  palmar  surface  of  the  left  hand,  and  sometimes  called 
warm  and  sometimes  cold  on  the  right  side.  Hot  is  called  cold  on  right  side  over 
the  areas  of  anaesthesia ;  not  so  on  the  left  side.  Can  distinguish  between  hot  and 
cold  test-tube  if  time  be  given  and  the  difference  great.  Almost  always  answers 
correctly  as  to  cold ;  often  does  not  feel  heat  at  all,  and  sometimes  calls  heat  cold, 
but  never  cold  heat.     Heat  and  cold  sense  normal  on  other  parts  of  the  body. 

Tactile  sense  on  right  arm  diminished  on  the  back  of  the  arm  and  radial  region 
of  the  forearm,  lost  on  the  back  of  the  hand  and  tips  of  the  fingers. 

On  left  arm  can  distinguish  between  sharp  and  dull  points  except  on  back  of 
hand  and  first  two  fingers. 

Tactile  sense  normal  on  the  left  little  finger. 

Sensation  to  pain  diminished  in  proportion  to  the  area  of  tactile  anaesthesia. 
The  position  of  the  arm  is  noted  well.     Muscular  sense  normal. 

BIBLIOGRAPHY. 

1.  Abbe,  Robert,  and  Coley,  W.  B. — Syringomyelia;  Operation,  Exploration  of 

the  Cord;  Withdrawal  of  Fluid,  Joum.  Nerv.  and  Ment.  Pis.,  1892,  p.  512. 

2.  Achard,  Ch. — Syringomyelic  avec  Amyotrophic  du  Type  Aran-Duchenne  et 

Anesthesie  dissociee  en  Band  Zosteroide,  Gaz.  hebdom.,  April  16,  1896. 

Syringomyelic,  Type  Morvan,  Gas.  des  Hopit.,  1891,  No.  82. 

Achard,  Ch.,  and  Joffroy.    See  Joffroy. 

3.  Adler—  Deutsche  med.  Woch.,  1893,  No.  18,  p.  432. 

4.  Agostini,  Cesare. — Rivista  sperimentale  di  Freniatria,  1894,  Fasc.  i. 

5.  Alelekoff,  A.  N. — Typic  and  Atypic  Forms  of  Syringomyelia,  Med.  Obozr., 

Moscow,  1894,  xli.  553-566. 

6.  Von   Ammon. — Die    angeborenen-chirurgischen    Krankheiten    des   Menschen, 

Berlin,  1842,  Tafel  xii.,  Fig.  13. 

7.  Andral. — Journal  de  Physiol,  exper.  (Obs.  124),  Paris,  1826. 

8.  Andresen,  F.  C. — Thesis  of  Kiel,  1869.     (Hydromyelia.) 

9.  Anfimoff. — Syringomyelic,  Type  Morvan,    Vestnik  Klin,  i  Sudibnoi  psichiat  i 

nevropatologii,  St.  Petersburg,  1891,  ix.,  Part  I.,  289. 

10.  Archangeli. — Presentezione  di   un   Malato   di   Syringomyelia,  Bull,   de  Soc. 

Lancisiana  d.  Osp.  di  Roma,  1891. 

11.  Arndt.— Munchener  med.  Woch.,  1892;  di  Roma,  1891,  308-324. 

12.  ASCH. — Neurolog.  Centralbl.,  1894,  p.  320.     (Discussion  with  Kupferberg.) 

13.  Asmus,  E. — Syringomyelia,  Bibliotheca  Med.,  Heft  1,  Cassel,  1893. 

14.  Aubert  und  Kammler. — Moleschott 's  Untersuchungen,  v.  p.  145,  1859. 

15.  Aufrecht.— Syringomyelic,  Path.  Mitt.,  Magdeburg,  1881,  184-187. 

16.  Baistrocchi. — Rivista  sperimentale  di  Freniatria,  1882,  Fasc.  iii.  p.  332. 

17.  Baker. — A  Case  of  Chronic  Anterior  Poliomyelitis  with  well-marked  Cutaneous 

Anaesthesia  and  Analgesia,  Brit.  Med.  Joum.,  Feb.  4,  1893. 

18.  Balmer. — Haut    Storungen    bei    Progressiver    Muskel    Atropine,  Archiv  fur 

Heilk.,  1875. 

19.  Bamberger.—  Wien.  med.  Presse,  1869,  No.  28,  p.  650. 

20.  Barbier,  C. — Sur  un   Cas  de   Syringomyelic,  Provence  Med.,  Lyon,  1889,  iii. 

376-379. 


SYRINGOMYELIA.  61 

21.  Bauhlnus,  Caspar. — Theatrum  Anatomicum,  Francfort,  1621,  lib.  iii.  p.  328. 

22.  Baumler,  Anna. — These  de  Zurich,  1887. 

Hohlenbildungen  im  Riickenmark,  Deutsch.  Arehiv  fur  hlin.  Med.,  xl.,  1887. 

Kranken  Yorstellung;    Slid- West  Deutsch.  Neurolog.,  etc.,  Neurolog.  Cen- 

Iralbl,  1890. 

23.  Bawli,  Jacob. — Syringomyelia  and  Trauma,  Konigsberg,  1896. 

24.  Becker. — Syringomyelic,  Arch.f.  Psychiatric,  Berl.,  1894,  xxvi.  601. 

25.  Beevor. — Tumors  of  the  Spinal  Cord  simulating  Syringomyelia,  Lancet,  Nov. 

18,  1893,  p.  1252,  also  Dec.  2,  1893. 

26.  The  Clinical  Society's  Transactions,  London,  1894. 

27.  Bexedikt. — Bemerkungen  zur  Demonstration  von  Weiss,  Wiener  med.  Doctoral 

Collegium,  1893. 

28.  Berbez,  P. — Essai  du  Diagnostic  d'une  Affection  inclependente  du  Tabes  avec 

Arthropathie  du  Coude  gauche,  France  Med.,  1885,  No.  97. 

29.  Berbez. — De  la  Syringomyelie,  Gaz.  hebdom.  de  Med.  et  de  Chir,,  Paris,  1889, 

xxvi.,  24  C. 

30.  Berkley,  H.  J.— -Brain,  London,  1889-90,  xii.  p.  460. 

31.  Bernhardt. — Beitrag   zur   Lehre    der    sogenannten    partiellen    Empfindungs 

Lahmung,  Berliner  hlin.  Wbch.,  No.  4,  1884.     (Bruhl,  Obs.  23.) 
— —Deutsch.  Archie  fur  hlin.  Med.,  vol.  xix. 
Contribution    to   the   Study   of    Partial    Paralysis   of    Sensibility    (Central 

Glioma  of  the  Cord),  Centralbl.  f.  Nervenheilkunde,  1887.     (  Vide  Bruhl,  Obs. 

21  and  22.) 

Syringomyelia  and  Scoliosis,  Centralbl.  f.  Nervenheilkunde,  No.  2,  1889. 

Ueber  die  sogenannte  Morvan'sche  Krankheit,  Deutsche  med.  Wbch.,  1891, 

19  Feb.,  p.  285. 
Litterarisch-historischer  Beitrag  zur  Lehre  von  der  Syringomyelic,  Deutsch. 

med.  Wbch. 

32.  Bernstein,  S.— O  Syringomyelic  Medycyna,  Warszawa,  1892,  xx.  167. 

33.  Bickeles.— Traumatic    Hsematomyelia  or  Syringomyelia,    Wiener  med.  Klub, 

8  Nov.,  1893. 
— —  Wiener  med.  Wbch.,  1893,  p.  1852. 

34.  Biernacki,  E. — Syringomyelic  Dissociation  of  Sensibility,  Gaz.  leharska,  War- 

saw, 1892,  2  S.,  xiii.  956-963. 
Neurolog.  Centralbl.,  1893,  p.  369. 

35.  Bjornstrom. — Algesimetrie,  Upsala,  1887. 

36.  Blocq,  Paul. — Demonstration  of  Syphilitic  Arthropathy,  Societe  d'Anatomie, 

1887. 

Brain,  1890,  Part  III. 

Gazette  des  Hopitaux,  Dec,  1889,  No.  140. 

Nouvelle  Iconographie  de  la  Salpetriere,  1889. 

Etudes  sur  les  Maladies  nerveuses,  Paris,  1894. 

37.  Boneti. — Sepulchretum,  Edit.  II.,  Geneva,  1700,  lib.  i.  p.  394. 

38.  Booth. — A  Case  of  Progressive  Muscular  Atrophy  with  Anaesthesia,  Medical 

Record,  N.  Y.,  1888. 

39.  I '.i:  am  well,  BYBOM. — Diseases  of  the  Spinal  Cord,  Lectures  23  and  24,  1895. 

40.  Bouchaud. — Syringomyelic  a  forme  de  Sclerose  laterale  amyotrophiqueet  Syrin- 

gomyelic complique  d'aiuesthesie  et  de  perte  du  sens  musculaire,  Echo  Midi- 
cale,  Toulouse,  1890. 

41.  BR]  a.vckau,  J. — Contribution  a  l'Etude  du  Champ  visuel  dans  la  Syringomyelic 

et  la  Maladie  de  Morvan,  These  de  Paris,  1891. 

42.  P.rissaud,  E. — Treatise  on  Diseases  of  the  Nervous  System,  Paris,  1895. 
Presse  medicate,  July,  1894. 

Rev.  neurologique,  Paris,  Oct.  15,  1894. 

Comptcj-Rendus  hebdomadaire  des  Seances  de  la  Societe  de  Biologie,  March 

15,  1895. 

43.  Broca. — Trophic  Scolioses,  Gazette  hebdomadaire  de  Mid.  et  de  Chirurg.,  No.  39, 

ISSN. 

44.  Bruce,  ALEXANDER. — Syringomyelia  in  a  Child,  Lancet,  June  16,  1894. 

45.  Bruhl,  I. — Contribution  a  L'Etude  de  la  Syringomyelic,  Paris,  1890. 

Manuel  de  Medecine,  Achard  et  Debove.     Article  on  Syringomyelia. 

De  la  Syringomyelie,  Archives  gen.  de  Midecine,  July,  Aug..  1889. 

La  Medecine  moderne,  Aug.  80,  1893. 

46.  Brunelle. — Syringomyelie:   fisemarthroses,   Bull.   Mid  du  Nord,  Lille,  1892, 

xxxi.  254,  279. 

47.  Brunner. — Misc.  Nat.  curios.,  1688. 


62  GUY    HINSDALE,    M.D. 

48.  Bruns. — Reference     to     Charcot's    Article     on     Syringomyelic    Arthropathy, 

Schmidt's  Jahrbiicher,  1894. 
Riickenmark's  Tumor,  Ncurologischc  Gentralblatt,  1894,  No.  7. 

49.  Brunslow. — Ueber   einige  seltene   Falle,  etc.  (Gliosis   Spinalis),  Berlin,   Dis- 

sert., 1890. 

50.  Bruttan,  C. — Casuistik  der  Syringomyelic,  Dorpat,  1892. 

Gesammte  Abhandlungen  aus  der  med.  Klinik  in  Dorpat,  1893. 

51.  Bull,  Edward. — Glioma  of  the  Cord,  Schmidt's  Jahrbiicher,  Bd.  cxciii. 

52.  Bullier. — Journ.  de  Phys.  exp'er.,  Paris,  1823,  Obs.  121. 

53.  Butz,  R.  V.— Chir.  vestnik,  St.  Petersburg,  1891,  vii.  508. 

54.  Bochroch,  M.  H. — Medical  News,  Philadelphia,  April  20,  1895. 

55.  Cacciola,  Salvatore. — Pathological    Histology  of  Syringomyelia,  Bollotino 

della  Reale  accademia  Medica  di  Roma,  t.  x.,  1887-1888. 

56.  Cagney,  James. — Syringomyelia  and  Morvan's  Disease,  Brain,  1891,  p.  368. 

57.  Caillet,  Frederic. — Etude  sur  les  Troubles  de  la  Sensibilite  dans  les  Affec- 

tions nerveuses  (Dissociation  syringomyelique),  These  de  Paris,  1891. 

58.  Calmeil. — Anatomie  et  Physiologie  de  la  Moelle  epiniere,  Journ.  de  Progres 

des  Sciences  et  de  VInstit.  med.,  t.  xi.  p.  77,  Paris,  1828. 
Ibid.,  1827,  p.  81. 

59.  Du  Castel. — Annales  de  Dermatologie,  v.  4,  April  and  May. 

60.  Chabanne. — Contribution  a  l'Etude  de  Hemiatrophie  de  la  Langue,  Thesede 

Bordeaux,  1892,  Obs.  14  and  15. 

61.  Charcot,  J.  B. — Revue  neurologique,  May  15,  1894. 

De  la  Dissociation  dite  syringomyelique  dans  les  Compressions  et  Sections 

des  Troncs  nerveux,  Mode  de    Retour  des    Sensibilites    apres   Operations. 
Compt.-Rend.,  Soc.  de  Biol.,  Paris,  1892,  iv.  941-45. 

62.  Charcot,  J.  M. — Lecons  sur  les  Maladies  du  Systeme  nerveux,  vol.  ii.,  Paris, 

1887. 

Maladie  de  Morvan,  Semaine  Med.,  ii.,  Dec,  1889. 

Un  Cas  de  Pseudo-Syringomyelie,  La  Semaine  Medicate,  1891,  p.  24. 

Lecons  du  Mardi,  t.  ii.,  1888-89,  21  St.  L. 

Clinique  des  Maladies  du  Systeme  nerveux,  t.  i.,  1892. 

Lecons  du  Mardi,  1890,  p.  488. 

De  la  Syringomyelic,  Bulletin  M'edicale,  28  Juin,  1889. 

Arthropathies  syringomyeliques,  Prog,  med.,  Paris,  1893,  2  S.,  xvii.  321-325. 

De  la  Maladie  de  Morvan,  Progres  medicate,  Dec.  11,  1889. 

Bull.  Med.,  Paris,  1889,  iii.  787. 

Echo  Med.,  Toulouse,  1890,  2  S.,  iv.  193,  205. 

Gaz.  hebd.  de  Med.,  Paris,  1891,  2  S.,  xxviii.  172. 

63.  Charcot,  J.  M.,  and  Brissaud. — Sur  un  Cas  de  Syringomyelic  observe  en  1875 

et  1890,  Progrhs  medicate,  24  Janvier,  1891,  No.  4. 

64.  Charcot  and  Joffroy. — Two  Cases  of  Progressive  Muscular  Atrophy,  Arch. 

de  Physiologie,  1870,  t.  iii.  p.  306. 

65.  Charcot  et  Brissaud.— Sur  un  Cas  de  Syringomyelic,  observe  en  1875  et  1890, 

Progrls  medical,  1891,  vol.  xxii. 

66.  Charcot  et  Hallion. — Sur  un  Cas  de  Paralysie  radiculaire  de  la  premiere 

Paire  dorsale  avec  Lesion  hemilaterale  de  la  Moelle  d'origine  traumatique 
simulant  la  Syringomyelic,  Arch,  de  Neurol.,  1891,  vol.  xxii. 

67.  Chantemesse. — Societe  medicale  des  Hopitaux  de  Paris,  Discussion  on  De- 

bove's  Case,  July  28,  1893. 

68.  Chauffard.— Soc.  med.  des  Hop.,  Nov.  4,  1892. 

69.  Cheron,  V.— Union  Medicale,  1889,  p.  685. 

70.  Chiari,   H. — Pathology   of   Syringomyelia,    Zeitschrift  f.   Heilkunde,    Prague, 

August,  1883. 

71.  Chipault. — Panaris  analgesique  avec  Fracture  spontanee;  Syringomyelic,  Bul- 

letin de  la  Soc.  anat.,  1890. 

72.  Cholschevnikoff. — Case  of  Peculiar  Reproduction  of  Peripheric  Nerve  in  De- 

generation of  a  Funiculus  in  Syringomyelia,  Med.  pribav  h.  morsk.  sborniku, 
St.  Petersburg,  1889,  174-194. 

73.  Church. — Syringomyelia,  Western  Medical  Reporter,  Chicago,  111.,  June,  1889. 

74.  Clarke,  Lockhardt,  and  Thudichum. — Beate's  Archives,  xiii.,  Obs.  2,  p.  41 ; 

Lancet,  vol.  i.,  1865,  p.  113. 

75.  Clarke,  L.,  and  Radcliffe. — On  the  Pathology  of  Tetanus,  Medico-chirurg. 

Trans.,  1865,  Case  II. 

76.  Clarke,  Lockhardt,  and  Hughlings  Jackson.— Medico-Chirurg.  Trans., 

1867,  p.  489. 


SYRINGOMYELIA.  63 

77.  Clarke. — Medico-Chirurg.  Trans.,  1868,  vol.  li. 

78.  Cohen,  S.  Solis. — Bulbar  Paralysis  with  Disturbance  of  Sensibility  to  Pain  and 

Temperature,  and  other  Symptoms  of  Syringomyelia,  Medical  and  Surgical 
Reporter,  July  13,  1889,  p.  34. 

79.  Coleman,  J.  P>.,  and  O'Carroll,  J. — A  Case  of  Syringomyelia,  Lancet,  Ausr. 

12,  1893,  p.  362. 

80.  Colleville. — Sur  un  Cas  de  Paresie  analgesique,  Gaz.  Jtebd.,  1887,  No.  25. 

81.  Critzman,  E.— Thesis  of  Paris,  1892. 

82.  Curschmann. — Klinische  Abbildungen,  Tafeln  17-23,  Berlin,  1894. 

83.  Czerny. — Ueber  neuropathische  Gelenkaffection,   Ccntralbl.  f.  Chirurgie,  1886, 

No.  24. 

84.  Dana,  C  L. — Case  of  Gliomatosis  of  the  Spinal  Cord  (and  Syringomyelia)  with 

Recurrent  Hemorrhages,  Journ.  of  Nerv.  and  Ment.  Lis.,  N.  Y.,  1894,  xxi. 
567-575  (January  and  October). 
New  York  Medical  Journal,  1893.     Also  Text-Book  on  Nervous  Diseases. 

85.  Daxenburger. — Ueber  Gliombildung  und  Syringomyelic,  Erlangen  Dissert., 

1890. 

Ueber  Compression-Myelitis,  etc.,  Deutsch.  Zeitsc.hr.  f.  Nervenheilk.,  Bd.  v. 

SO.  Debove. — A  Case  of  Syringomyelia,  Bull,  de  la  Soc.  med.  des  Hopitaux,  Feb. 

22,  1889. 

Gaz.  hebdom.,  1889,  No.  10. 

Maladie  de  Morvan  on  Lepre,  Soc.  med.  des  Hopit.  de  Paris,  July  20,  1893. ' 

87.  Dejerine. — Sur  un  Cas  de  Syringomyelic  suivi  d'Autopsie,  Semaine  Med.,  June 

12.  1889. 

Bull,  de  la  Soc.  med.  des  Hopitaux,  Feb.  22,  1889. 

Compt.-Rend.  de  la  Soc.  de  Biol.,  Paris,  1890. 

88.  Dejerine  and  A.  Thuilaxt. — Dissociation  of  Thermic  Sensibility  in  a  Case 

of  Syringomyelia,  with  Autopsy,  La  Medecine  moderne,  Feb.  5,  1891. 

89.  Dejerine. — Retrecissement  du  Champ  visuel  dans  la  Syringomyelic,  Soc.  de 

Biol.,  July  12,  1890. 

90.  Dejerine  and  Sottas. — Syringomyelic  unilaterale,  Le  Bulletin  medical,  1892, 

p.  1102. 

91.  Dejerine  et  Mirallie. — Hemiatropia  de  la  Face  avec  Phenomenes  oculo- 

pupillaires  dans  un  Cas  de  Syringomyelic  unilaterale. 

Troubles   trophiques   et  vaso-moteurs   dans  la  Syringomyelic,  Archives  de 

Physiologic,  Oct.,  1895. 

92.  Dejerine  and  Letulle.— La  Maladie  de  Friedreich,  La  Semaine  Mid.,  1890. 

93.  De  Jong. — Progressive  Bulbar  Paralysis  in  a  Case  of  Syringomyelia,  Freiburger 

Dissertation,  1889. 

94.  Dercum,  F.  X. — International  Clinics,  vol.  ii.,  1892. 
Journ.  Nerv.  and  Mr,,/.  Dis.,  March  and  April,  1894. 

95.  Dercum  and  Spiller. — Amer.  Journ.  Med.  Sciences,  Dec,  1896. 

96.  Desnos   and   BaBINSKI. — Bull,  et  Mem.   Soc.   med.  des  Hop.  de  Paris,  1891, 

652-656. 

97.  Dickinson. — On  the  Pathology  of  Chorea,  Med.-Chirurg.  Trans.,  vol.  lix.  p.  3, 

1876. 

98.  DONATH. — Ueber  die  Grenzen  des  Temperatursinnes,  etc.,  Arch.  f.  Psych.,  Bd. 

xv,  1884. 

99.  Dreschfeld. — Some  Rare  Forms  of  Muscular  Atrophy,  Brain,  1885. 

100.  DuCHENNE   DE   BOULOGNE. — De  l'Electrisat.  localisee,  3d  ed.,  vol.  i.  p.  453, 

Paris,  1847. 

101.  Duesing,  Hermann.— Pathologisch-anatomische  Untersuchung  eines   Falles 

von  Syringomyelic,  Wlirzburg,  L891,  Stael,  28  pp. 

102.  During,  E. — Lepra  und  Syringomyelie,  Deutsch.  med.  Woch.,  1894,  No.  ti. 

103.  Dyer,  Isidore. — Syringomyelia  and  Lepra  Nervorum,  New  Orleans  Med.  and 

Sur,,.  .Journ.,  Aug.,  IS',12. 

104.  EdgewORTH. — Bristol  Medico- Chirurgical  Journ.,  Jan.,  1894. 

105.  Eiieers. — Lepra  and  Syringomyelia,  /."  Semaine  Med.,  1893,  No.  56. 

106.  BiCHHORSi    \m>  N\("nvn.     Arch./,  exper.  Path,  und  Phar.,  t.  ii.,  1S74. 

1 07.  Eickholt.  -Contribution  to  the  Study  of  Central  Sclerosis,  Arch.  /'.  Psychiatric, 

1NXO,  t.  x.  p.  61 3. 

108.  Eisenlohr.-  -Zur  pathol.  Anatomic  der  syphilitischen  Tabes;  Syringomyelie, 

. !/•'■//.  /'.  Psychiatric,  Bd.  xxiii.  p.  603. 

Neurol.  Centralbl,  L892,  p.  453. 

Lin  Fall  von  Moivan'-clirr  K rankheit,  Deutsch.  und.  Woch.,  1S93. 

109.  Erb. — Krankheiteu  des  Riickenmarks,  Ziemssen's  Bandbucher,  xi. 


64  GUY    HINSDALE,    M.D. 

Erb.— Neurol.  CentralbL,  1893,  No.  6,  p.  177. 

110.  Erben. — Internal,  klin.  Rundsch.,  May,  1892. 

111.  Eskridge,  J.  T. — International  Clinics,  vol.  iv.,  3d  Series,  Phila. 
International  Clinics,  vol.  ill.,  2d  Series. 

112.  Eulenberg,  Albert.— Berlin  klin.  Woch.,  1869,  No.  44;  ibid.,  1866,  No.  46. 
Study  of  the  Methods  of  Examination  of  Sensibility,  Zeitschr.  f.  klin.  Med., 

ix. ;  Real  Encyklopadie,  1889. 

113.  Eulenberg. — Deutsch.  med.  Woch.,  Dec.  14,  1893. 

114.  Fambourere,  P. — Archives  de  Neurologie  (of  Moscow),  1893,  xxvi.  134. 

115.  Fedoroff,  M.  J. — Un  Cas  de  Syringomyelic,  type  Morvan,    Yuzh  o  Russko 

Med.  Gaz.,  Odessa,  1893,  pp.  479-493;  Rev.  neurologique,  1893,  p.  634. 

116.  Ferrannini,  Andrea. — Nucleo  nosologico  della  siringomielia  definito  da  una 

sua  forma  familiare  sinora  non  descritta,  La  Ri/orma  medica,  Anno  x.,  Nos. 
136-140,  1894. 

117.  Ferrier,  D. — Localization  of  Atrophic  Paralyses,  Brain,  vol.  iv.,  1881. 

118.  Fischer,  Heinrich. — Zur  Casuistik  und  Diagnose  der  Syringomyelic,  Inaug. 

Dissert.,  Leipzig,  1894. 
Zeitschr./.  Chirurg.,  Bd.  xii. 

119.  Francotte,  X. — Formation  Gliomateuse  d'une  Cavite,  Arch,  de  Neurologie, 

1890,  No.  56. 

120.  Freund. — A  Case  of  Muscular  Atrophy  with  Disorders  of  Sensibility,  Wiener 

med.  Woch.,  Nos.  13  and  14,  1885,  p.  390.     (Bruhl,  Obs.  26.) 

121.  Friedmann. — Archiv  /.  Psychiatric,  xvi.,  1885. 

122.  Friedreich. —  Virchow's  Archiv,  Bd.  xxvi.,  1863,  p.  410. 

123.  Frommann. — Untersuch.  uber  norm.  u.  path.  Anat.  d.  Riickenmarks,  I.  Theil, 

Jena,  1864,  p.  79. 

124.  Furstner    and    Stuhlinger. — Ueber    Gliose  und    Hohlenbildung    in   der 

Gehirnrinde,  Arch./.  Psychiatrie,  Bd.  xvii.  p.  1. 

125.  Furstner  and  Zacher. — Pathology  and  Diagnosis  of  Cavities  of  the  Spinal 

Cord,  Arch./.  Psychiatrie,  1883,  p.  433,  v.  xiv.     (Bruhl,  Obs.  25.) 

126.  Funke.—  Ueber  eine  neue  Methode  zur  Prufung  des  Temperatursinnes,  Zeitschr. 

/.  Heilkunde,  Bd.  xi.,  1890. 

127.  Galezowski. — Disturbances  of  Vision  in  Syringomyelia,  Rev.  d' Ophthalmol., 

Paris,  1893,  xv.  546-551. 

128.  Galloway.— Brit.  Med.  Journ.,  1891,  p.  641. 

129.  Geimelli. — Pseudo-Syringomyelie,  etc.,  dans  la  Paralysie  generale  (Artefacts), 

Rivista  sperimentale  di  Freniatria,  vol.  vii.,  Fasc.  1,  33d  yr. 

130.  Gerlach,  Wold. — Ein  Fall  von  congenitaler  Syringomyelic  mit  intramedul- 

larer  Teratombildung,  Deutsches  Zeitschr./.  Nervenheilkunde,  1894,  p.  271. 

131.  Gessler,  H. — Syringomyelia  and  Morvan's  Disease,  Med.  Cor.  Bl.  d.  Wiirtem- 

berg.  Arztl.  Ver.,  Stuttgart,  1893,  lxiii.  1-6. 

132.  Gignon. — Traite  de  Medecine,  vol.  vi.,  Paris,  1894. 

133.  Gimeno,  A.— Caso  notable  de  Siringomyelia,  Progreso  med.-/arm.,  Madrid,  1891, 

iv.  479. 

134.  Glaser. — Central  Angeiosarcoma  of  the  Cord,  Archiv  /.  Psychiatrie,  1885,  xvi. 

p.  85. 

135.  Goldscheider.— Verhandlungen  der  physiologischen  Gesellschaft  zu  Berlin, 

seance  14  Mars,.1890. 

Archiv  /.  Psychiatrie,  xviii.,  1887. 

Berlin  klin.  Woch.,  1892  (Discussion). 

Arch.  v.  Dubois-Reymond,  1885. 

136.  Gombault. — Lepra  et  Syringomyelic,  Revue  neurologique,  1892. 

Sur  un  Cas  de  Maladie  de  Morvan,  Gaz.  des  Hopit.,  1889,  No.  50. 

Revue  neurologique,  1893,  No.  14. 

Un  Cas  de  Maladie  Morvan,  suivi  d'Autopsie,  Gaz.  hebd.,  1889,  Nos.  19 

and  20. 

137.  Gortz—  Ueber einen  Fall  von  Syringomyelic,  Inaug.  Dissert.,  Greifswald,  1892. 

138.  Gowers. —  ClinicalJournal,  London,  May  31,  1893. 

Diseases  of  the  Nervous  System,  1st  ed.,  1888. 

Clinical  Lectures,  Philadelphia,  1895  (Lecture  xii.). 

139.  Graf,  E. — Neurologisches  CentralbL,  1893,  p.  699. 

140.  Grasset. — Lecons  sur  le  Syndrome  bulbo-medullaire,  Montpellier  Med.,  1889. 
Un  Cas  de  Maladie  de  Morvan,  Lecons  recueillies,  Paris,  1892. 

141.  Gray,  Landon  Carter. — Treatise  on  Nervous  Disease  and  Insanity,  2d  ed. 

1895,  Philadelphia,  p.  282. 
Boston  Med.  and  Surg.  Journ.,  1890,  p.  570. 


S  Y  HIS  GUM  Y  ELI  A .  6  5 

142.  Grimm,  J. — Muscular  Atrophy,  Virchow's  Archiv,  1869,  xlviii.  445. 

143.  Guixox. — Traite  de  Medecine,  Edited  by  Brissaud,  vol.  vi.,  chapter  ou  Syrin- 

gomyelia, Paris,  1894. 
Nouvelle  Iconographie  de  la  Salpetriere,  iii.,  1890. 

144.  Guelliot. — Panaris  analgesique,  Gaz.  hebdom.,  1886. 

14").  Gull,  Sir  Wm.,  axd  Clark. — A  Case  of  Progressive  Muscular  Atrophy  of  the 
Hand,  with  Dilatation  of  the  Central  Canal  and  Atrophy  of  the  Gray  Matter, 
Guy's  Hospital  Reports,  1862,  p.  244. 

146.  Guxther. — The  Typical  Form  of  Progressive  Muscular  Atrophv,  Berlin,  hlin. 

Woch.,  1883. 

147.  Gyubmann. — A  Case  of  Syringomyelia,  Wiener  med.  Presse  (Bruhl,  Obs.  33), 

u.  Pesther  med.  Presse,  1889. 

A  Case  of  Syringomyelia;  Post-mortem  Examination,  Ungarisches  Archiv 

fur  Medizin,  Bd.  i.  Heft  1,  1892. 
Festschrift  an  Prof.  Koranyi,  1891. 

148.  Hadlich. — Neurologisches  Centralbl.,  Dec,  1887,  p.  558. 

149.  Halliox,   Louis. — Thesis  of  Paris,  1892,  Mevue  ncurologique,  Feb.  28,  1893; 

Neurologisches  Centralblatt,  No.  4,  1892;  ibid.,  No.  20,  1892. 

150.  Hallopeau,  H. — Contribution  to  the  Study  of  Diffuse  Periependymal  Sclero- 

sis, Gaz.  mid.  de  Paris,  No.  1,  1870. 

151.  Haxot. — Paresie  analgesique  a  Panaris,  Arch.  gen.  de  Med.,  1877. 

152.  Hansen. — La  Semaine  Medicate,  1893,  No.  56,  p.  447. 

153.  Harckex,  Justus.— Thesis  of  Kiel,  1883. 

154.  Harris. — ISote  on  a  Case  of  Multiple  Tumors  of  the  Cord  and  of  the  Brain, 

with  a  Contribution  to  the  Pathology  of  Syringomyelia,  Brain,  1886,  vol.  vii. 
p.  447. 

155.  Haumaxx,  Emil. — Thesis  of  Greifswald,  1889. 

156.  Hebald,  Otto. — Arch.  /'.  Psychiatrie,  Bd.  x. 

1"»7.  HegemaNN,  Paul.— Thesis  of  Bonn,  1889,  Case  III. 

158.  Hellick. — Contributions  to  the  Etiology  of  Syringomyelia,  Sborn.  lek.v.Praqe, 

1890,  iii.  487-550. 

159.  HEBING. — Temperatursinn,  Hermann's  Handbuch  der  Physiologic 

160.  Herold. — Glioma  of  the  Cord,  Arch./.  Psychiatric,  xv.,  1884. 

161.  Hertzex. — On  the  Separation  of  the  Thermic  Sense  into  Two  Distinct  Senses, 

Pfliiger's  Arch.,  xxxviii. 

162.  Hinsdale,  Guy. — Ixterxatioxal  Medical  Magazixe,  Nov.  and  Dec,  1896, 

Jan.,  1897. 

163.  HlTZlG. — Arch.f.  Psychiatric,  xvi.,  1885,  p.  566. 

Hematorrhachis  Syringomyelia,  etc.,  Allg.  Zeitschrift  f.  Psychiatrie,  Berlin. 

1885,  p.  702. 

164.  Hochenegg-Paltauf. — Ueber    symmetrische    Gangran,     Wiener    met.    Jahr- 

biicher,  1885. 

165.  Hochhaus,  H. — Zur  Kenntniss  des  Ruckenniarks  Gliom,  Dcutsches  Archiv  f. 

/.■/in.  Med.,  Bd.  xlvii.  p.  603. 

166.  Hoffmaxx,  Johann.— Neurol.  Centralbl.,  1889,  No.  19. 

Sainmlung  klin.  Vort.  von  Volkmann,  1891,  No.  20. 

Deutsches  Zetischr.f.  Nervenheilkunde,  Bd.  iii.,  1892. 

167.  HOLSCHEWNIKOFF. — A  Case  of  Syringomyelia  with  Degeneration  of  the  Pe- 

ripheral Nerves  and  Trophic  Changes  (Acromegaly),  Virchoto's  Archives,  No. 
11'. i,  iss.-,. 

168.  HOMEN,  E.  A. — Bidrag  till  kennedoms  zur  Syringomyelin,  Nonl.  Med.  Arc/tie, 

vol.  xxvi.,  No.  1,  1894. 

169.  Huckel.— Minichener  med.   Woch.,  Nos.  27  and  28,  1889. 

170.  Hutin. — Nouv.  Bibliothegue  mid.,  t.  i.  p.  159,  Paris,  1828. 

171.  Holt,  L.  Emmet,  and  C.  A.  Hebteb. — Acute  Gliomatosis,  Amer.  Journ.  M"l. 

Sci.,  April,  1895. 

172.  HUBLEB,  W.— Inaug.  Dissert.,  Wi'irtzbnrg,  1S!»4. 

173.  Jackson,  BuGHLINGS,  AND  GALLOWAY. — Lancet,  1892. 

174.  Jacquet.    -Soc.  '!<■  Biologie,  1890. 

175.  Jacquet  et  8aint-Gebmain. — L6siona  cavitairea  de  la  Moelle  dans  tm  ("as  de 

Sclerodermic,  Sue.  francaise  de  Derm,  et  (]>•  Syphilogr.,  April  22,  1892. 

Lesions  cavitaires  de  la  .Aloell<>  dans  un  ( 'as  de  SiN'ri.dennie,  BOC.  lianeaise 

de  Derm,  et  de  Syphilogr.,  April  22,  1892. 

176.  Jeffries,  John  Amoby.    Journ.  Ment.  and  Nerv.  Dw.,  Sept.,  1890. 

177.  Jimkno,  A.     Caso  notable  de  SyriiiLromielia,  Qorresp.  Mtd.,  .Madrid,  1894,  xxix. 

228-230. 


66  GUY    HINSDALE,    M.D. 

178.  Joffroy  axd  Achard. — Myelitis  with  Cavities,  Arch,  de  Physiologic,  1887. 

179.  Joffroy. — Syringomyelie  non-gliomateuse  associee  a  la  Maladie  de  Basedow, 

Archives  de  Med.  e.vp'er.  et  cl 'Anatomic palhologi que,  1891,  p.  90. 

180.  Joffroy,  A.,  et  Achard,  Ch. — Syringomyelie  non-gliomateuse  associee  a  la 

Maladie  de  Basedow,  Neurol.  Centralbl,,  1894. 
Nouvelle  Autopsie  de  Maladie  de  Morvan,  Syringomyelic,  Archives  de  Med. 

exp'er.  et  d'Anatomie  pathologique,  1891,  p.  677. 

Inflammation  de  l'Ependyme  de  la  Moelle  epiniere,  ibid.,  Jan.,  1895. 

Ibid.,  1890,  p.  540. 

181.  Joffroy,  A.— Bull,  et  Mem.  de  la  Soc.  des  Hop.,  1891,  p.  92 ;  and  1889. 

182.  Jolly,    F. — Ueber   trophische   Storungen    bei    Riickenmarks   Erkrankungen, 

Char  ite- Annate  n,  Berlin,  1891,  336-349;  also  Archiv  f.  Psychiatrie,  Berlin, 
1891,  585. 

183.  Journ.  de  Medecine  de  Bruxelles,  1893,  No.  22  (Review). 

184.  Juman. — La  France  Medicale,  Paris,  1890. 

185.  Kahler,  M. — Cervical  Paraplegia  with  Unusual  Disturbances  of  Sensibility, 

Prager  med.  Woch.,  x.  18,  1882.     (  Vide  Bruhl.) 
The  Diagnosis  of  Syringomyelia,  Prager  med.  Woch.,  No.  6,  1888.     (  Vide 

Bruhl.) 
Two  Cases  of  Syringomyelia,  La  Semaine  Medicale,  1888,  p.  83. 

186.  Kahler  and  Pick. — Contribution  to  the  Study  of  Syringomyelia  and  Hydro- 

myelia,  Prager  Vierteljahrschrift,  cxlii.,  1879. 

Arch.  f.  Psychiatrie,  x.,  1880. 

Beitrag  zur  Pathologie  und  pathologischer  Anatomie  des  central  Nerven- 

systems,  Leipzig,  1879. 

187.  Kanasugi,  H. — Casuistische  Beitrage  zur  Kenntniss  der  Syringomyelie,  Er- 

langer  Dissert.,  1890. 

188.  Karg. — Zwei  Falle  von  ausgedehnten  neuropathischen  Knocken  und  Gelenk- 

zerstorungen,  Arch./,  klin.  Med.,  Bd.  xli.  p.  101. 

189.  Kesteren. — Pathological  Histology  of  the  Cord,  St.  Bartholomew's  Hosp.  Repts., 

1872. 

190.  Kethi  —  Wiener  med.  Woch.,  1890,  No.  26. 

191.  Kiewlicz,  Marian. — Deutsches  Arch.f.  Psychiatrie,  xx.,  1888. 

192.  Klebs,  E. — Glioma  of  the  Spinal  Cord,  Prager  Vierteljahrschrift,  exxxiii.,  1877, 

Obs.  1,  p.  74. 

193.  Klemm. — Arthritis  deformans  bei  Tabes  und  Syringomyelie,  Deutsch.  Zeitschrift 

f.  Chirurgie,  Bd.  xxxix. 

194.  Klippel. — Les  Lesions  de  la  Moelle  dans  la  Scoliose  de  l'Enfance,  Gaz.  hebdom,, 

1891,  No.  13. 

195.  Knoppek. — Beitrae   zur   Diagnostik   der   Syringomyelie,    Wiener  med.  Presse, 

1892,  No.  3,  or  Wiener  med.  Woch.,  1892. 

196.  Koberlin. — Hohlenbildung  im  Riickenmark,  Munch,  med.  Woch.,  1889,  No.  19. 

197.  Kohler,  Hermann. — Meningitis  Spinalis,  Leipzig,  1861,  p.  105. 

198.  Koppen. — Acute  Cavity  Formation  in  the  Spinal  Cord,  Neurologisches   Ccn- 

tralblatt,  1892,  p.  487. 

199.  Korb. — Syringomyelia  and  Degeneration  of  the  Posterior  and  Lateral   Col- 

umns; Autopsy,  Deutsch.  Zeit.f.  Nervenheilk.,  Bd.  viii.,  1896,  p.  359. 

200.  Kornfeld. — Tabes  with  Symmetrical  Gangrene  and  Symptoms  of  Syringo- 

myelia, Wiener  med.  Woch.,  Nov.  5,  1892. 

201.  Kornilow—  Neurol.  Centralbl,  1892,  p.  493. 

202.  Krafft-Ebing. — Allg.  Wiener  med.  Zeilung,  1892,  No.  48. 

203.  Krauss,  E. — A  Case  of  Syringomyelia,  Virchoiv's  Archives,  Bd.  c,  1885. 

204.  Krauss,  W.  C. — Journ.  Nerv.  and  Merit.  Bis.,  Nov.,  1892,  p.  304. 

205.  Kretz,  R.— La  Semaine  Med,,  Feb.,  1890  ;    Wien.  Uin.  Woch.,  1890,  pp.  479-500. 

206.  Kbonig—  ZeiUchr.f.  klin.  Med,,  Bd.  xiv. 

207.  Kronthal. — Contribution  to  the  Study  of  the  Pathology  of  Cavities  in  the 

Spinal  Cord,  Neurologisches  Centralbl.,  N on.  20-22,  1889. 

208.  Kupferberg,  Heinz. — Ei ii  unter  dem  Bilde  eines  Gehirntumors  verlaufender 

Fall  von  chronischen  idiopathischen  Hydrocephalus  internus,  complicirt 
mit  symptomloser  Syringomyelie,  Deutsch.  Zeitschr.f.  Nervenheilkunde,  1893, 
p.  94." 

209.  Lachmann. — Gliom  im  obersten  Theile  des  Filum  terminale,  Arch.f.  Psychia- 

trie, Bd.  xiii- 

210.  Lamacq. — Journ,  de  Med.  de  Bordeaux,  1889-90,  xix.  361. 

211.  Lancereaux. — A  Case  of  Hypertrophy  of  the  Spinal  Ependyma  with  Oblit- 

eration of  the  Central  Canal  of  the  Cord,  Bull,  de  la  Soc.  de  Biologie,  t.  iii. 
p.  224,  1862. 


SYRINGOMYELIA.  67 

212.  Landois  and  Mosler. — Study  of  the  Dissociated  Troubles  of  Sensibility,  Ber- 

liner Hin.  Woch.,  1868.     (Bruhl,  Obs.  36.) 

213.  Langhans,  Th. — On  the  Formation  of  Cavities  in  the  Cord  following  Hemor- 

rhage, Virchow's  Archives,  Bd.  lxxxv.,  1881. 

Zur  Casuistik  der  Riickenmarksaffection  (Tetanie  und  Lepra  ana?sthetiea), 

Virchow's  Archives,  1875,  p.  175. 

214.  Lassala,  A.—  Cron.  med,,  Valencia,  1892,  pp.  353-358. 

215.  Leegaard,  C. — Gliomatosis ;  Syringomyelia  seated  in   the  Posterior  Horns, 

Norsk.  Mag.f.  Laege-vidensk,  Christiania,  1890,  v.  69-84. 

Method  of  Examining  Sensation  of  Temperature,  Deutsch.  Archiv  f.  klin. 

Med.,  1891,  Bd.  xlviii.  3.  und  4.  Heft.  p.  207. 

216.  Lefort. — Panaris  analgesique,  Mercredi  Medical,  Dec.  30,  1890,  p.  651. 

217.  Lemoine. — On  Syringomyelia,  Gaz.  med.  de  Paris,  12-14,  1889. 

218.  Lenhossek. — Oesterr.   Zeitschr.  f.  prakt.  Heilk.,  Jahr  V.,  Vienna,  1859,  pp. 

62-63. 

219.  Lenz,  G.— Thesis  of  Freiburg,  1892. 

220.  Lepine. — Syringomyelia,  Lyon  Medical,  1892,  lxxi.  481. 

221.  Letjbe. — Methods  for  Examining  Sensibility,  Ccntralhl.f.  die  med.  Wissenschaft., 

1876. 

222.  Levi  et  Sauvineau. — Syringomyelia  with  Reflex  Iridoplegia,  Le  Mercredi 

Med.,  1895,  No.  15,  p.  173. 

223.  Leyden. — Hydromvelus  and  Syringomyelia,  Virchow's  Archives,  Bd.  lxviii.,  1»76, 

pp.  1-11. 
Klinik  der  Riickenmarks-Krankheiten,  vol.  ii.,  1875,  pp.  452-454. 

224.  Lloyd,  Jas.  Hendrie. — Arthropathy,  etc.,  Philadelphia  Hospital  Reports,  1892. 
Trans.  Coll.  Phys.,  Phila.,  1893,  Univ.  Med.  Mag.,  March,  1893. 

Traumatic  Affections  of  the  Spinal  Cord  Simulating  Syringomyelia,  Journ. 

Nerv,  and  Ment.  Bis.,  June,  1894. 

225.  Looft. — Lepra  besonderes  Riickenmarks,  Virchow's  Archiv,  Bd.  cxxviii. 

226.  Loubovitch,  J. — Memoires  M'edicaux,  Moscow,  1894,  Nos.  1  and  2. 

227.  LUNN,  J.  R.,  and  Beevor.— Lancet,  May  19,  1894. 

228.  Lunenburg,  J. — A  Case  of  Hydro-Syringomyelia,  Gazeta  lekarska,  1894,  No.  13. 

229.  Lorenti. — Riforma  Medica,  1894. 

230.  Londe  and  Perry. — Nouvelle  Iconographie  de  la  Salpetriere,  July  to  Oct., 

1894. 

231.  McConnele,  J.  W. — Two  Cases  of  Syringomyelia:  One  of  Unilateral  Type, 

Journ.  Nerv.  and  Mod.  Dis.,  April,  1894. 

232.  Mader. — Hydromyelia  generalized  throughout  the  Cord,    }\iencr  Med.  Blatt., 

1885. 

233.  Magelhaes. — Lepra  e  siringomielia,  Gaz.  Med.  da  Bahia,  Maio,  1894,  No.  14. 

234.  Mann,  Ludwig. — Zwei  Falle  von  Syringomyelic  nebst  Bemerkungen  uber  das 

Vorkommen  des  tabischen  Symptom-Complexes  bei  derselben,  Deutsch.  Arch, 
f.  klin.  A  led.,  1892. 

235.  Marestang. — Contribution  a  l'Etude  du  Diagnostic  diffcrentiel  de  la  Lupre 

ansesthesique  et  de  la  Syringomyelic,  Revue  de  Aled.,  Paris,  1891,  xi.  781. 
Ann.  de  Der.  et  de  Syphilogr.,  1892,  p.  407. 

236.  Marie. — Un  Cas  de  Syringomyelic  a  Forme  pseudo-acromegalique  (Cheiro- 

megalie),  La  Semaine  Medicate,  1S!)4,  Nos.  22  and  23. 

237.  Marinesco,  G. — Contribution  a  la  Pathologie  des  Arthropathies  neuro-spinabs, 

Hi  rue  ncurologique,  July  30,  1894. 
Archives  de  Physiologie,  .July,  1893,  No.  3. 

238.  Martin. — Transactions  of  the  Eleventh  International  Medical  Congress,  Rome, 

1894. 

239.  MARWEDEL,  Q.— Munchen.  med.   Woch.,  1890,  xxxvii.  810. 

240.  Masius.— Un  Cas  de  Syringomyelic,  Liittich,  1890. 

241.  Mennicee,  <  >. — Ueber  Syringomyelia  mit  anatomischer  Untersuchung,  zweite 

Falle,  Marburger  Dissert,  1891. 

242.  Meyer,  Ludwig. —  Virchow's  Archives,  Bd.  x.wii.,  1863,  p.  414. 
Canadian  Practitioner,  July  16,  1892. 

243.  Mi'.ykks.  I).  C— Canadian  Practitioner,  1892,  p.  321. 

244.  Mills,  ('has.  K. — Town.  Nerv.  mid  Ment.  Dts.,  April  and  June,  1894. 

245.  Minor. — Arch./.  Psychiatrie,  vol.  xxiv. 

Contribution  a  l'Etude  oVHematomyeiie  et  de  la  Syringomyelic,  Congrea  de 

Berlin,  Aug.,  L890,  and  Semaine  Midicale,  Aug.  6,  1890.  ' 

Neurol.  Centralbl,  1890,  No.  Hi. 

Neurol.  Centralbl,  1894. 


68  GUY    HINSDALE,    M.D. 

246.  Miura,  Kiunosuke. — The  Origin  of  Cavities  in  the  Cord,  Virchow's  Archives, 

Bd.  cxvii.,  1889. 

247.  Ueber  Gliorn  des  Riickenmarks  und  Syringomyelie,  Neurol.   Centralbl,  1892, 

No.  4. 

248.  Monod  ET  Keboul. — Contribution  a  l'Etude  de  Panaris  analgesique  (Maladie 

de  Morvan),  Archiv.  gen.  de  Med.,  1888,  p.  28. 

249.  Moore. — Dilatation  of  the  Central  Canal  of  the  Cord,  Trans.  Path.  Soc.,  Lon- 

don, Oct.,  1880. 

250.  Morgagni  and  Santorini. — Leyden.  1740,  Animadvers.  xiv.,  pp.  17-18. 

251.  MORVAN.—  Oaz.  hebdom.  de  Med.  et  de   Chirurg.,  1883,  No.  35;  1886,  No.  32; 

1887,  p.  549. 

De  l'Ansesthesie  sous  les  divers  Modes,  etc. ;  Cas  frustes  de  Pareso-analgesie, 

ibid.,  1889,  Nos.  35  and  36. 

252.  Muller,  Hermann  F. — Deulsches  Arch./,  kiln.  Med.,  1894,  vol.  Hi.  p.  259. 

Internal  klin,  Rundschau,  1893. 

253.  Muller,  Friedrich. — Ein  Fall  von  Syringomyelic,  Berlin,  klin.  Woch.,  1894, 

No.  12. 

254.  Muller,  Fr.,  ttnd  Meder. — Zeitschri/t  /.  klin.  Med.,  1895,  Bd.  xxviii.  p.  47. 

255.  Muller,  Carl. — Ein  Fall  von  Morvan'sche  Krankheit,  Deutsch.  Med.  Woch., 

1895,  No.  13. 

256.  Naunyn.—  Centralbl.  f.  d.  med.  Wiss.,  1894,  No.  6. 

257.  Neuberger. —  Wiener  med.  Presse,  1894,  No.  12,  p.  445. 

258.  Neuhaus,  Hugo.— Thesis  of  Berlin,  1889. 

259.  Newmark,  Leo.— Medical  News,  July  22,  1893,  p.  88. 

260.  Nissen,  F. — Syringomyelic  Arthropathy,  Arch.  /.  klin.  Chirurg.,  Berlin,  1892- 

93,  xlv.  204-220. 

261.  Nonat. — Researches  on  the  Development  of  an  Accidental  Canal  in  the  Spinal 

Cord,  Arch,  gen,  de  Med.,  1838,  p.  287. 

262.  Nonne,  M. — A  Case  of  Typical  Tabes  Dorsalis  and  Central  Glioma  in  a  Syph- 

ilitic, Arch.  /.  Psychiatrie,  Berlin,   1892,  xxiv.  526-533;  Neurol.   Centralbl., 
1892,  p.  453. 

263.  O'Connor. — A  Case  of  Syringomyelia  with  Symptoms  of  Neuritis  of  the  Left 

Brachial  Plexus,  Hahnemannian  Medical  Monthly,  Philadelphia,  1890. 

264.  Ollivier. — Traite  de  la  Moelle  epiniere  et  de  ses  Maladies,  1823. 

265.  Oppenheim,  H. —  Charite-Annalen,  1885,  p.  409. 

A  Case  of  Syringomyelia,  Neurol.  Centralbl,  1884.     (Bruhl,  Obs.  27.) 

Arch./.  Psychiatrie,  xv. 

Arch./.  Psychiatrie,  xxv.,  1893,  p.  315. 

266.  Osler. — Glioma  of  the  Spinal  Cord,  Journ.  Nerv.  and  Ment.  Dis.,  1888. 

267.  Ormerod,  J.  A. — A  Case  of  Spinal  Disease,  Probably  Syringomyelia,  Trans. 

Med.  Soc,  London,  1891,  xv.  452. 

268.  Pagenstecher. — -Syringomyelie,    Spina     Bifida,     angeboren     Hydromyelus, 

Zeitschr./.  klin.  Med.,  Bd.  xxii. 

269.  Pellizi. — A    Case   of    Pellagra   with    Syringomyelia,   Rivista  sperimentale   di 

Freniatria  e  di  Med.  legale,  t.  xviii.  f.  iii.  et  iv. 

270.  Parmentier. — Nouvelle  Iconographie  de  la  Salpetriere,  1890,  p.  213. 

271.  Pennato,  P. — Syringomyelia  e  Tumori  Spinali,  Riv.  renatadi  Sc.  med,,  Venezia, 

1894,  xx.  485. 

272.  Perves. — Contribution  a  l'Etude  comparee  de  la  Syringomyelie  et  la  Maladie 

de  Morvan,  Bordeaux  Thesis,  1891. 

273.  Preobrajenski,  P.  A. — Un  Cas  de  Syringomyelie  non-gliomateuse,  Memoires 

mhlicaux,  Nos.  12  and  14,  1894. 

274.  Perrey. — Arthropathies  of  Syringomyelia,  Paris  Thesis,  1894. 

275.  Peterson,  Frederick. — Acromegaly  combined  with  Syringomyelia,  Medical 

Record,  New  York,  Sept.  23,  1893. 

276.  Ppeiffer. — Ein    Fall  von    ausgebreitetem   ependymaren    Gliom  der  Gehirn- 

hohlen,  Deutschcs  Zeitschr./.  Nervenheilk.,  1894,  p.  459. 

277.  Piccolhuomini. — Anatomical  prcelectiones,  Rome,  1856,  p.  260. 

278.  Pick.—  Arch./.  Psychiatrie,  viii.  285,  1878;    Wiener  med.  Woch.,    1888. 

279.  Pingen,  K. — Zur  Casuistik  zur  Syringomyelie,  Seven  Cases,  Three  with  Au- 

topsy, Inaug.  Dissert.,  Cologne,  1894. 

280.  Pitres  and  Sabrazes. — Bacteriological  Examination  of  the  Spinal  Cord  and 

Nerves  in  Syringomyelia,  Arch.  klin.  de  Bordeaux,  May,  1893. 

Systematic  Nervous  Leprosy,  Syringomyelic  Type,  Nouvelle  Iconographie 

de  la  Sal  pfi  trie  re,  No.  3,  1892. 

281.  Portal. — Mem.  sur  la  Nature  et  le  Traitement  de  plusieurs  Maladies,  Paris, 

1800,  vol.  i.  p.  53. 


SYRINGOMYELIA.  69 

282.  Portal  et  Senac. — Cours  d'Anatom.  med.,  t.  iv.  p.  117,  Paris,  1804. 

283.  Pospelow. — Lepra  und  Syringomyelic,  Monats.  f.  prakt.  Derm.,  Bd.  xv.  1892, 

p.  81. 

284.  Prexant. — Sur  le  Canal  ependymaire  primitif,  Intern.  Monatschr.f.  Anat.  und 

Phys.,  1894. 

285.  Prince,  Morton*. — Article  in  "  Nervous  Diseases  by  American  Authors,"  ed- 

ited by  Dercum,  Philadelphia,  1895. 

286.  Pkibram—  Praqer  med.  Woch.,  1891,  No.  24. 

287.  Prus.— Przeglad  lekarski.  Krakow,  Nos.  48-52,  1893. 

Syringomyelic  und  Morvan'sche  Krankheit  und  Lepra,  Areh.f.  Psychiatrie, 

1895,  t.  xxvii.  fasc.  iii. 

288.  Eachetti.— Delia  Struttura  della  Aledul.  Spinal,  Milan,  1816. 

289.  Eaichlixe,  A. — Contribution  a  l'Etude  clinique  de  la  Syringomyelic  sur  un 

Cas  de  Syringomyelic  avec  Manifestations  bulbaires,  Paris,  1892. 

290.  Eaichlixe,  A.,  et  Gulnost,  Geo. — Progris  med.,  1891,  No.  4,  p.  83. 

291.  Eaxvier. — On  the  Neuroglia,  Acad,  des  Sciences,  June  5,  1882. 

292.  Eauzier.— -Now.  Montpellier  Med.,  1893,  t.  ii. 

293.  Eaymoxd. — Note  on  a  Case  of  Hydromyelia,  Arch,  de  Physiologie,  1888. 
Anatomie  pathologique  du  Systeme  nerveux. 

Atrophies  musculaires  et  Maladies  amyotrophiques,  1889. 

Archives  de  Neurologie,  Aug.,  1893. 

294.  Eedlich,  Emile. — Zur  pathologischen  Anatomie  der  Syringomyelie  und  Hy- 

dromyelie:    aus  dem   Labor,  von  Prof.  Obersteiner  in  Wien,  Neurol.    Gen- 
tralbl.,  1892,  No.  4. 

295.  Eeisixger  und  Marchaud.—  Virchow's  Archiv,  Bd.  lxviii.,  1884,  p.  369. 

296.  Eemak.— A  Case  of  Syringomyelia,  Deutsch.  med.   Woch.,  No.  47, 1884.    (Bruhl, 

Obs.  28.) 

Berliner  J:lin.  Woch.,  1887. 

Areh.f.  Psychiatrie,  vol.  ix. 

Oedema  of  the  Superior  Members  of  Spinal  Origin,  Berliner  klin.  Woch.. 

No.  3,  1889.     (Bruhl,  Obs.  24.) 

297.  Eexaut. — Arch,  de  Physiologie,  1882. 
Gaz.  mhl.  de  Paris,  1884. 

298.  Eiesinger.— Glioma  of  the  Cord,  Virchow's  Archives,  xcviii.,  1884. 

299.  Ripping. — Allgemeine  Zeitschrift  f.  Psychiatrie,  vols.  xxx.  and  xxxii.,  1874  and 

1875. 

300.  Eoger.— Revue  de  Medecine,  1892,  p.  577. 

301.  Eosenbach. — The  Diagnosis  of  Syringomyelia,  Petersburc/  med.   Woch.,  No.  9, 

1887.     (Bruhl,  Obs.  34.) 
On  the  Neuropathic  Symptoms  of  Lepra,  Neurol.  <  'entralbl.,  No.  16,  1884. 

302.  Eosenbach  und  Schtscherbak.— Zur  Casuistik  der  Syringomyelie,  Neurol. 

Gentralbl,  1890. 

303.  Rosenblath.— Deutsche*  Areh.f.  klin.  Med.,  1893,  Bd.  Ii.  p.  210. 

304.  Eoss  and  Thorburn.— On  the  Segmentary  Distribution  of  Sensory  Disturb- 

ances, Brain,  1NXS. 

305.  Eoss,  J. — A  Case  of  Syringomyelia,  Treatise  on  Diseases  of  the  Nervous  Sys- 

tem, vol.  i.,  London,  1883. 

306.  ROSSOLIMO,  G.  J.—  Gentralbl.  f.  Nerrenheilkunde,  1889;  Neurol.  Gentralbl.  1892. 

No.  15,  p.  493. 
Zur  Physiologie  der  Scleife,  Areh.f.  Psychiatrie,  Bd.  xxi.  p.  897. 

307.  Roth,  Vladimir.— Diffuse  (Miosis  of  the    Cord,  Syringomyelia,   Muscular 

Atrophy,  Archives  </>■  Physiologie,  1878. 

On  Medullary  Gliomatosis,  .ir<-/i.  de  Neurologic,  lsxy,  l.xss. 

Archives  <!<■  Neurologie,  xiv.-xvi,  1887-89.     (For  Cases  1  and  2  of  Roth, 

see  Bruhl,  Obs.  30  and  31.) 

Beceuil  des  Travaus  de  Neuropathologie  et  de  Psychiatrie  decliee  par  ses 

eleves  a  M.  le  Prof.  Kojewnikow,  Moscow,  1890. 
— — Archives  de  Physiol,  norm,  etpath.,  t.  v.,  Paris,  1S78. 

Neurol.  Centralbl.,  1892,  p.  ■!!>:;. 

"us.  Rouffiet. — Essai   clinique  sur   le   r&recissemenl   du  Champ  visuel  dans  la 

Syringomyelie  el  dana  la  Maladie  de  Morvan,  Thesis  of  Paris,  L890. 
309.  Rtjllieb. — Destruction  of  a  Greal   Pari  of  the  Cord,  with  Contracture  of  the 
Arm  and  Perfed   Mobility  of  the  Lower  Extremities,  Journal  de  Physiologie 
experimental,  L823. 
810.  Rumpf.    -Neurol.  Centralbl.,  L889,  Nas.  7  and  1<». 


70  GUY    HINSDALE,    M.D. 

311.  Rummo,  G.,  of  Pisa.— Leziono  di  clinica  Medica,  vol.  i.,  Naples,  1891;   Terapia 

clinica,  1893,  No.  2. 

312.  Rumpf.— A   Case  of  Syringomyelia,   etc.,    Neurol.    Centralbl.,    1889.      (Bruhl, 

Obs.  29.) 

313.  Sachs,  B.,  and  Armstrong.— New  York  Med.  Journ.,  April  30,  1892. 

314.  Sachs,  B.— New  York  Med.  Journ.,  1888. 

315.  Santangelo,  F. — Caso  clinico  di  Syringomyelia  con   Manifestazione  tardive 

della  Malattia  di  Morvan,  Pisani,  Palermo,  1891,  xii.  185-199. 

316.  Sander. — Arch./.  Psychiatrie,  xi.,  1880. 

317.  Sass,  A.  von. — Zvvei  Falle  von  Lepra  nervorum,  Arch.f.  klin.  Med.,  Bd.  xlvii. 

318.  Sohaffer,  C,  and  Preiss,  H.— Ueber  Hydro-  und  Syringomyelic,  Arch.  f. 

Psychiatrie,  Bd.  xxiii. 

319.  Schlesinger,  H.— Zur  Casuistik  der  partiellen  Empfindungslahmung  (Syrin- 

gomyelic), Wiener  med.   Woch.,  1891,  Nos.  10-14. 
Beitrage  zu  den  Sensibilitats-Anomalien  bei  Lepra  ansesthetica,  Deutsche 

Zeitschr.f.  Nervenkr.,  Bd.  ii.  p.  230. 

Symptomatology  of  Syringomyelia,  Neurol.  Centralbl.,  1893,  pp.  684-688. 

Neurol.  Centralbl.,  1893,  No.  3;  Revue  neurologique,  1893,  p.  25. 

Centralbl./.  Nervenheil  kunde  und  Psychiatrie,  March,  1894,  p.  151. 

Prayer  med.  Woch.,  1892,  xvii.  585. 

Monograph  on  Syringomyelia,  Leipsic  and  Vienna,  1895. 

320.  Schmidt,    Adolf. — Doppeltseitige    Accessoriuslahmung    bei    Syringomyelic, 

Deutsch.  med.  Woch.,  1892,  No.  26. 

321.  Schmidt,  Max.— Inaug.  Dissert,  Munich,  1894. 

322.  Schmitt  AND  Baraban.— A  Case  of  Syringomyelia,  Rev.  med.  de  I'Est,  1888. 

323.  Schultze,  Fr. — Ueber  Spalthohlen  und  Gliombildungim  Ruckenmark,  Archiv 

von  Virchow,  1882,  t,  lxxxvii.     (  Vide  Bruhl.) 

Arch.f.  Psychiatrie,  Bd.  viii.,  1878. 

Beitrag  zur  Lehre  von  der  centralen  Gliose  des  Ruckenmark  und  Syringo- 
myelic, Archiv  von  Virchow,  cii.  1885.     (  Vide  Bruhl.) 

Klinisches  und  anatomisches  iiber  Syringomyelic,  Zeitschr.  f.  klin.  Med., 

xiii.,  1888,  p.  523.     (  Vide  Bruhl.) 

Zur  kenntniss  der  Lepra,  Deutsches  Arch.f.  klin.  Med.,  xliii.,  1888. 

Deutsch.  med.  Woch.,  1893,  No.  46. 

324.  Schull  —  Deutsches  Arch.f.  klin.  Med.,  xx.  p.  271,  1877. 

325.  Schuppel,  O.— Hydromyelia,  Arch.  d.  Ifeilkunde,  1865,  p.  289. 

Glioma  of  the  Cord,  Arch.  d.  Heilkunde,  p.  113,  1867. 

A  Case  of  Generalized  Anaesthesia,  1874. 

326.  Seebohm—  Tumor  of  the  Cord  with  Syringomyelia,  Thesis  of  Strasburg,  1888 

or  1889. 

327.  Seeligmuller.— Ueber  Syringomyelic.  Miinchener  med.  Woch.,  1891. 

328.  Shaffer,  Karl,  and  Dr.  Hugo  Preiss. — Hydromyelus  und  Syringomyelic, 

Arch.f.  Psychiatrie  u.  Nervenkr..  xxiii.  1-39. 

329.  Shaw,  J.  C— New  York  Med.  Journ.,  1890. 

330.  Silcock.— Syringomyelia,  Path.  Soc.  of  London,  vol.  xxxix.,  Jan.,  1888,  and 

British  Med.  Journ.,  1888. 

331.  Simon,  Th.— Arch.f.  Psychiatrie,  1875,  p.  120,  Obs.  1,  2,  3,  4,  8. 

332.  Singer,  J. — Two  Cases  of  Syringomyelia,  Prayer  med.  Woch.,  1892,  xvii.  537. 
Prayer  med.  Woch.,  1891,  No.  45. 

333.  Sinkler,  Wharton.— International  Clinics,  vol.  iii.,  3d  Series,  Philadelphia, 

1893. 

334.  Simon. — Syringomyelia  and  Tumors  of  the  Spinal  Cord,  Arch.f.  Psychiatrie,  v., 

1875. 

335.  Spiller,  W.  G. — Traumatism  and  Hsematomyelia  a  Cause  of  Syringomyelia, 

International  Medical  Magazine,  April,  1896,  p.  193. 

336.  Spiller  and  Dercum. — Trans.  Amer.  Neurological  Association.,   1896,  and 

Amer.  Journ.  Med.  Sciences,  Dec,  1896. 

337.  Sokoloff. — Two  Cases  of  Glioma  of  the  Central  Nervous  System,  Deutsch. 

Arch.f.  klin.  Med.,  t.  xli.,  1887. 

Arthropathy  in  Syringomyelia,  Vratch,  1891. 

Deutsche  Zeitschrift  f.  Chirurgie,  1892,  Bd.  xxxiv. 

338.  Sonnenberg.— Arthropathies,    Berliner   klin.    Woch.,  Nov.    27,  1893;    Lancet, 

June  2,  1894., 

339.  Souqtjes,  A. — Etude  sur  les  Syndromes  hysteriques  simulateurs  des  Maladies 

de  la  Moelle  epiniere,  These  de  Paris,  1891. 

A  Case  of  Syringomyelia,  Type   Morvan,   Nouvelle   Iconographie   de  la 

Salpetriere,  Paris,  1892,  v.  286-291 ;  also  Neurol.  Centralbl,  No.  4,  1892. 


SYRINGOMYELIA.  71 

340.  Souza- Martin,  of  Lisbon. — International  Medical  Congress,  Rome,  1894,  La 

Semaine  Medicate,  1894,  No.  20. 

341.  Von  Spanje.—  Weekblatt  van  het  nederl.  Tijehr.f.  Geneesk,  1893,  a  1,  No.  18. 

342.  De  Speville  —  Morvan's  Disease,  Thesis  of  Paris,  1888. 

343.  Stadelmann. — Deutsches  Arch./.  klin.  Med.,  xxxiii.,  1883. 

344.  Standhartner. — Jahresber.   des   alleem.  Krankhauses   in  Wien   vom  Jahre 

1891. 

345.  Starr,  M.  Allen. — Amer.  Journ.  Med.  Sci.,  May,  1888. 

346.  Stembo,  L. — St.  Petersburger  wed.  Wbch.,  1892,  No.  35. 

347.  Sterne. — On  Syringomyelia,  Indiana  Med.  Journ.,  Indianapolis,  1893-94  pp 

187-195. 

348.  Steudener. — Syringomyelia  in  Lepra  Mutilans,  Obs.  1,  p.  7,  Erlangen,  1867. 

349.  Strumpell,  A. — Glioma  of  the  Cervical  Cord,  Deutsches  Archie  /'.  klin.  Med 

xxviii.,  1881. 

Archivf.  Psychiairie,  x.,  1880,  p.  695. 

450.  Steno. — Central  Glioma  of  the  Spinal  Cord,.s7.  Thomas's  Hospital  Reports  1885 
London,  1886. 

351.  Tambourer.— Neurol.  Centttdbl,  1892,  p.  494. 

352.  Tanzi. — La  Siringomielite  nella  Patologia  nervosa  e  nellesue  Applicazioni  alia 

Fisiologia,  Qaz.  d.  Osp.,  Napoli,  1891,  xii.  571-573. 
Rivista  sperimentale  di  Freniatria  ecc.,  1890,  fasc.  iv. 

353.  Taylor,  James.— Lancet,  Jan.  28,  1893,  p.  286. 
Gumma,  British  Medical  Journal,  1883. 

Syphilitic  Meningitis;  Gumma  and  Cavity  in  the  Cord,  Trans.  Path.  Soc. 

of  London,  xxxv.,  1884. 

354.  Tcherkassow,  T.,  Mhnoirex  uddieau.r,  1894,  No.  8. 

355.  Thibierze,  G. — Les  Alterations  cutanees  de  la  Syringomyelic,  Ann.  de  Derm. 

et  de  Syphilogr.,  Paris,  1890,  3  S.,  i.  799-813. 

356.  Thomas. — Syringomyelia  in  a  Child  set.  6  [Hydromyelia?],  Medical  News  Dec 

21,  1895;  Lancet,  Dec.  14,  1895. 

357.  Thomson,  Alexis. — Edinburgh  Hospital  Reports,  vol.  ii.,  1894. 

358.  Tornow.— Berlin  Dissertation,  1863  (Diagnosis). 

359.  Tornu,  E.— Ann.  Assist. pub.  Buenos  Aires,  1891-92,  ii.  281-296. 

360.  Tourette,  Gil  les  de  la. 

361.  TURNER,  Charlewood.— Syringomyelia  with  Dilatation  of  the  Cerebral  Ven- 

tricles, Trans.  Path.  Soc,  London,  1888. 
British  Medical  Journal,  1887,  p.  1281. 

362.  Turner,  W.  A.,  and  Ashley,  W.  Mackintosh.— Three  Cases  of  New  Growth 

with  Cavity  Formation  in  the  Cord,  Brain,  Parts  LXXIV.  and  LXW 
1896,  p.  301. 

363.  Upson,  H.  S.— A  Case  of  Syringomyelia,  New  York  Medical  Journal,  Aug.  31, 

1889. 

364.  Vandervelde. — Anatomie  normale  et  pathologique  du  Canal  centrale  de  la 

Moelle  epiniere,  Jour,  de  Mid.  et  de  Chirurgie et  de  Pharmacologic,  ism,  No.  22. 

365.  Van  Gieson,  Ira. — Tourn.  Nerv.  <tu<l  Ment.   Dis.,  July,  1889,  and  New   York 

Mot.  Journ.,  vol.  ii.,  1889. 

366.  Vassale,  G.  (Regqio).— Italian  Congress  "di  Freniatria." 

367.  La  VeCCHIA,  L. — Syringomyelia    and    Morvan's    Disease,   Lavori   di    Com:,   di 

Med.  inter.,  Milan".  1893,  198-211  ;  Munchener  med.   Wbch.,  Dec.  27,  1892^ 

368.  Vergelly. — De  la    Dissociation  syringomyelique  de  la  Sensibilite  chez  lea 

Diabetiques,  Gaz.  hebdom.  de  Med.  et  dr  Chirurg.,  1893,  No.  32. 

369.  Verhoogen. — Tourn.  dr  Mid.,  dr  Chirurg.,  et  dr  Pharm.,  1893,  No.  22. 

370.  Verhoogen  et  VanderVelden. — Annates  des  Sciences  midicalea  et  nat- 

urelles,  Bruxelles,  1894,  iii. 

371.  Vesely.— Soc.  dea  ftfexlecins  de  Prague,  Feb.  12,  1894. 
872.  Vierordt.— Zeitschrift  f.  Biologic,  lid.  12. 

273.  Vixai.is,  Fr. — El Progreso  meaico-farmac.,  1893. 

374.  Volkmann,  R. — Beitrag  zur  Lehre  vor  dem  Gliom  und  der  secondaren   De- 
generation <les   Etiickenmarks,  etc.,  Deutsches  Arch.  /'.  klin.  Med.,  Bd    xlii 
L888,  p.  433. 

875.  Vought,  Walter.     New  York  Medical  Journal,  June  11, 1891,  liv.  561   564. 
New   )'"/■/•  Medical  Journal,  .Ian.,  1892. 

376.  Vii.i'iAx.  -Arch,  dr  Physiol.,  t.  ii.,  L869,  |>.  637. 

■  <:i.  Wehlau,  I,.    -Medical  Record,  Dec.  12,  L891. 

378.  Weintraud,  W. — Zwei    Falle  von  Syringomyelic  rait   Posticuslahmung  und 
Cucularisatrophie,  Deutsches  2kitschr.  f.  Nervenheilkunde,  1894,  p.  383. 


72  SYRINGOMYELIA. 

379.  Westphal,  C.— A  Case  of  Tumor  and  of  Cavities  of  the  Cord  with  Alteration 

of  the  Medulla  Oblongata,  Arch.  /'.  Psychiatrie,  1875,  t.  v.  p.  90;  Brain,  vol. 
vi.,  July,  1883. 
-Contribution  to  the  Study  of  Syringomyelia,  Brain,  1883. 

380.  Whipham.— Glioma  of  the  Cord  with  Dilatation  of  the  Central  Canal,  Trans. 

Path.  Soc.  of  London,  March,  1881,  and  Lancet,  1881,  p.  418. 

381.  Wichmann,  Ealf.— Ueber  Gesehwulst  und  Hohlenbildung  im  Riickenmark, 

Tubingen,  1887  (32  cases),  Stuttgart,  1887.     (  Vide  Bruhl.) 

382.  Weiss — Bevue  neurologique,  1893,  p.  137. 

383.  Zambaco-Pacha. — Les  Lepreux  de  la  Bretagne;  communic.  faite  a  l'Academie 

de  la  Medecine,  Aug.  23,  1892,  Paris,  Masson. 

384.  Zambaco.—  La  Sentaine  Medicate,  1893. 

385.  Zambaco   et   G.   Thibierge.— Lepre    ansesthesique   et   Synngomvelie,    Gaz. 

hebdom.,  1891,  No.  2. 

386.  Ziehl—  Deutsch.  med.  Woch.,  1889,  No.  17,  p.  335. 

Addendum. 

387.  Dimitroff,  Stephan  (of  Adrianople,  Turkey). — Archiv  fur  Psychiatrie  und 

Nervenlcranhheiten,  xxviii.  Bd.  2  Heft  and  xxix.  Bd.  1  Heft,  Berlin,  1896,  82  pp. 
This  essay  contains  a  valuable  synopsis  of  297  cases  hitherto  published,  classi- 
fied in  four  groups. 

388.  Saxer,  F.  (of  Marburg). — Beitrage  zur  pathologischen  Anatomie  und  zur  allege- 

meinen  Pathologie,  xx.  Bd.  2  Heft,  Jena,  1896,  66  pp. 

Total  References,  514. 


NDEX.1 


Acrodynia,  47. 

Acromegaly,  54. 

Agostini,  50. 

Alcohol  a  cause,  40. 

Amblyopia,  35. 

Analgesia,  43. 

Aran-Duchenne,  18. 

Arterial  circulation,  4(3. 

Arthritis  deformans,  28. 

Arthropathy,  22-29. 

Aspiration  of  joint,  24. 

Atrophies,  18. 

Bulbar  symptoms,  35. 

Cancer,  54. 

Cavity,  8. 

Cervical  pachymeningitis,  54. 

Cheiromegaly,  54. 

Circulation  in  the  spinal  cord,  46. 

Clark's  column,  12,  49, 

Cold,  sense  of,  32,  47,  59. 

Cystitis,  33. 

Definition,  4. 

Derivation,  3. 

Dermographism,  32. 

Development,  6. 

Diagnosis,  52,  54. 

Dissociation  symptom,  37,  55. 

Kffusion  into  joint,  24. 

Electrical  reactions,  19. 

Embryology,  5. 

Embryonal  cells,  G. 

Erythromelalgia,  47. 

Etiology,  45. 

Excision  of  shoulder,  24. 

Eyes,  3:;. 

Ferrannini,  47. 

Fibrillary  tremors,  19. 

Formication,  47. 


Fracture,  30. 

Friedreich's  ataxia,  54. 

Gait,  19. 

Gangrene,  20,  22. 

Glioma,  15. 

Heredity,  46 

Histology,  5. 

Hydromyelia,  4. 

Hyperesthesia,  51. 

Hypnotism,  50. 

Hysteria,  50. 

Infection,  20,  57. 

Infectious  disease  a  cause,  46. 

Knee-jerk,  44,  56,  58. 

Laryngeal  palsy,  36 

Latent  form,  50. 

Lateral  sclerosis,  43. 

Leprosy,  51. 

Lloyd,  8,  12,  27,  37. 

Macroscopic  appearances,  8. 

Marinesco,  25,  27. 

Melancholia,  54. 

Meninges,  31. 

Mesoblast,  G. 

Morgagni,  3. 

Morvan's  type,  48. 

Mouth,  21. 

Myelite  cavitaire,  4,  15,  38. 

Myelosyringosis,  4. 

Nerve-supply  of  articulations,  21 

Neuritis,  15. 

(Edema,  21,  :'.::. 

Ollivier,  8. 

<  teteoma,  29. 

Fain,  dermal,  18. 

Pathoiogy,  8. 

Pemphigus,  20,  21. 

Portal,  3. 


1  For  authors'  name-,  see  Bibliography. 


7;; 


74 


INDEX. 


Position  of  cavity.  10. 
Posterior  sclerosis,  13,  44,  48. 
Pupils,  33. 

immobility  of,  34. 
Rachetti,  3. 

Reaction  of  degeneration,  19. 
Santorini,  3. 
Scoliosis,  31. 

Sensory  symptoms  absent,  3G. 
Souza-Martin,  52,  53. 
Spastic  symptoms,  43. 
Sphincters,  33. 
Spinal  column,  30,  53. 


Spinal  fluid,  15. 
Stilling,  3. 
Symptom  atology,  17. 
Syphilis,  46,  51,  56. 
Temperature,  surface,  22. 
Thermo-ana3sthesia,  39. 
Tongue,  21. 
Trauma  a  cause,  45. 
Trophic  changes,  20. 
Ulcerations,  20. 
Varieties  of  syringomyelia,  47 
Vasomotor  disturbances,  32. 
Visual  fields,  34. 


Hinsdale 
S^ingongrelia, 


RC^06.S9 
1897 


